Unit 7 Sex Determination

UNIT 7
SEX DETERMINATION

Structure
7.1 Introduction 7.6 Sex-Limited and Sex-
Enfluenced Traits
Objectives
Sex-Limited Traits
7.2 Genetic Basis of Sex
Determination Sex-Influenced Traits

Genic Type 7.7 Dosage Compensation

Chromosomal Type In Man

7.3 Chromosomal Sex In Drosophila

Determination Mechanisms
7.8 Summary
The XX-XY System
7.9 Terminal Questions
A Variation: The ZZ-ZW System
7.10 Answers
The XX-XO System

Sex Determination by Ploidy

Level

The Compound Chromosome

System

The Transfer Gene

7.4 The Chromosome Tneory of

Inheritance and Sex-Linkage
7.5 Sex-Linked Inheritance
X-Linked Traits in Humans

Y-Linked Traits in Humans

7.1 INTRODUCTION
One of the probable deductions from your study of Mendel’s laws of
inheritance and their extensions and modifications in Units 1 and 2 may be
that contribution to inheritance is equal from both the parents. But sex linkage
is a major exception to it. Sex linkage occurs when a gene controlling a trait is
located on the sex chromosome. The sex chromosome bears several genes in 183
Block 2 The Physical Basis of Heredity
addition to those directly concerned with sex determination. The inheritance of
these genes follows a characteristic pattern which is different from that seen in
the examples of monohybrid and dihybrid inheritance, that you have studied
so far. The unique sex-linked pattern(s) of inheritance of any particular trait
can be easily recognised and studied by pedigree analysis.

Sex linkage forms the main theme of this unit. But we begin by a brief
discussion on mendelian factors that we now know are the genes and are
located on the chromosomes. Then you will study examples of genes located
on the sex chromosomes and their mode of transmission to the next
generation. These would be explained with examples of X-, and Y-linked
genes. This is followed by a subsection dealing with sex determination in
eukaryotes, which involves both environmental and genetic factors. Next, you
would study the genetic basis of sex determination, which is either of genic
type or of chromosomal type.

Objectives
After studying this unit you would be able to:

distinguish between the genic and chromosomal type of sex

determination,

describe the chromosomal sex determination mechanisms,

relate the chromosome theory of inheritance to sex linkage,

distinguish the mode of inheritance between the X-linked genes and Y-

linked genes,

explain with the help of examples the transmission of recessive and

dominant X-linked traits,

explain with examples the transmission of Y-linked genes,

discriminate between sex-limited and sex-influenced genes, and

enumerate their role in the control of secondary sexual characters,

explain the importance of dosage compensation mechanism,

differentiate between the type of dosage compensation in mammals

and Drosophiia, and

describe the existence of female mosaics with respect to X-linked

traits.

7.2 GENETIC BASIS OF SEX DETERMINATION

In most organisms, the sex determining mechanism is under genetic control,
free of environmental factors. In the genome of higher organisms, there are
certain genes or chromosomes which regulate-sex determination and thus sex
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is determined at the time of fertilisation.
Unit 7 Sex Determination
7.2.1 Genic Type
In some organisms, certain independent genes located on different
chromosomes are responsible for sex determination. Most species of fish
illustrate this mode. The male may be represented as AA1 for the sex
determining genes, and the female as AA (Fig. 7.1). According to this
assumption, maleness is determined by the gene A1 which is dominant over A.

In a parasitic wasp, called Habrobracon, genes are responsible for sex

determination in a different way. The sex determining gene has multiple alleles
(Xa, Xb, Xc, Xd). When two alleles in a zygote are different or heterozygous
(XaXb, XaXc, XbXc, etc.) a normal, fertile female is formed. If the alleles in the
Fig. 7.1: Sex
zygote are in homozygous (XaXa, XbXb, etc.) or hemizygous (Xa, Xb, etc.) determination in fish at
condition males are formed. genic level.

7.2.2 Chromosomal Type

It refers to the condition where the genes involved in sex determination are
located on specific chromosomes known as the sex chromosomes.

First, we shall see how the genic type of sex determination evolved into a
chromosomal type of sex determination mechanism. In the primitive forms, the
only difference between the two sexes was in their gametes. Later in
evolution, morphological or phenotypic difference developed in the two sexes
of a species.

In primitive forms, sex determination was due to genes on autosomes (the

genic type). In the process of evolution, gradually, the genes responsible for
sex determination got localised on specific chromosomes - the sex
chromosomes. These chromosomes were designated as ‘X’ and ‘Y’ or ‘Z’ and
‘W’ and they can usually be distinguished morphologically from each other.
The remaining chromosomes of the complement are known as ‘autosomes’
and are designated ‘A’.

The X and Y chromosomes differ from each other in many respects. This is
because, there is accumulation of sex determining genes on the respective
sex chromosomes. Also, there is negligible crossing-over between the X and Y
chromosomes. This helps to preserve gene combinations favouring distinct
sexual differences. The consequence is that the Y chromosome bears mostly
the genes essential for the male determination while all the other genes
become inert. These regions got reduced in size in some species and are
completely lost in others. This was how the heteromorphic sex chromosome
evolved.

7.3 CHROMOSOMAL SEX DETERMINATION

MECHANISMS
In most of the higher plants and animals, the chromosomal sex determination
mechanisms are prevalent. Basically, five types of' chromosomal mechanisms
exist. These are XX-XY, ZZ-ZW, XX-XO, ploidy level, and compound
chromosome system. 185
Block 2 The Physical Basis of Heredity
7.3.1 The XX-XY System
This is a common mode of sex determination in animals including man and
some plants like the angiosperm genus Lychnis (see details in subsection
3.5.1). Both the sexes have equal number of chromosomes, of which one pair
is of sex chromosomes. In females, the two sex chromosomes are similar and
are called the X-chromosomes. Thus, the female is the homogametic sex
(‘homo’ meaning same). Males in contrast usually possess an X chromosome,
and one chromosome is dissimilar in morphology from all others and is known
as the Y chromosome. Because the male sex chromosomes are different, the
male is called the heterogametic sex (‘hetero’ meaning different).

In humans, the characteristic diploid chromosome number is 46 (Fig. 7.2). The

females have 22 pairs of autosomes (AA) and a pair of X chromosomes (AA +
XX). The males have 22 pairs of autosomes (AA) alongwith an XY pair (AA +
XY). The sperms formed are either X-bearing or Y-bearing. This sex is
determined by the sperm because all eggs are similar and X-bearing. Studies
on sex chromosomal abnormalities in man, helped in understanding the crucial
role of Y-chromosome in determining maleness. It has been observed that a
single Y chromosome, irrespective of the number of X-chromosomes present
in the zygote, causes an individual to develop into a phenotypic male. And in
the absence of a Y-chromosome, the zygote leads to femaleness. Genes on
Fig. 7.2: The XX-XY the Y chromosome direct differentiation of the embryonic gonad to a testis,
system of sex whose hormonal products then induce a male phenotype. Genes on the Y
determination in man. chromosome also control spermatogenesis. Thus, the presence of the Y
chromosome determines maleness, and without a Y chromosome, the female
phenotype develops.

7.3.2 A Variation: The ZZ-ZW System

Under this system, the male is the homogametic sex and the female is
heterogametic. In order not to confuse this type of sex determination with the
XX-XY mechanisms, the male chromosomes are labelled ZZ, the female ZW.
In this system the ovum determines the sex of the resultant offspring, because
all sperms carry similar chromosomes. Other than the reversal of homo-, and
heterogametic sexes, the ZZ-ZW system functions similar to the XX-XY
system. This mode of sex determination has been observed in birds including
domestic fowl (see Fig. 7.3), butterflies and moths, some fishes, reptiles and
amphibians, and in a plant species Frageria orientalis.

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Fig. 7.3: The ZZ-ZW system of sex determination in domestic fowl.
Unit 7 Sex Determination
7.3.3 The XX-XO System
In some species, the two sexes have different numbers of chromosomes. The
difference often involves the sex determination mechanism. This phenomenon
is called the XX-XO system (O indicates the absence of one sex
chromosome). The female has two sex chromosomes just as in the XX-XY
system, but the male has only one and is thus designated XIO. In the species
exhibiting this system, the diploid number of the chromosomes in male is one
less than that of the female as a result of the absence of one sex
chromosome. Consequently, the number of chromosomes is odd in males and
even in females. The grasshopper (Fig. 7.4) is a good example of this mode of
sex determination. The cricket and the beetle also exhibit a similar
chromosomal basis of sex determination.

7.3.4 Sex Determination by Ploidy Level

In many species of hymenoptera (bees and wasps) and some mites and ticks,
sex is determined by the number of sets of chromosomes or ploidy of the
individual. Females are diploid, producing haploid gametes via meiosis. Most
Fig. 7.4: The XX-XO
eggs are fertilized by haploid sperm from males, but a few are not. The
system of sex
fertilised eggs become females that show biparental inheritance. While the
determination in
unfertilised eggs develop into haploid males (by parthenogenesis) that inherit grasshopper.
their genes exclusively from their mother (Fig. 7.5). Haploid individuals, of
course, cannot undergo normal meiosis, so males produce gametes via
mitosis.

Fig. 7.5: Sex determination by ploidy level in honeybee.

Because males do not undergo meiosis for gamete production, all the sperms
from one individual are genetically identical to each other and to the male
parent. This has the interesting consequence of increasing the gametic
relatedness of a male’s daughters. Remember in this system, a male produces
no sons - only daughters. On an average, all daughters of one mated pair of
bees share 75% of their genes, rather than the normal 50% relatedness of 187
Block 2 The Physical Basis of Heredity
offspring of most species. The daughters are identical for all the 50% of the
genes received from their father, plus one-half of the 50% of the genes from
their mother, this makes a total of 75% genetic relatedness.

In some vertebrates also unusual degrees of ploidy are associated with a

particular sex. Some species of lizards consist of mostly triploid (3N) females
and few males. In fact, males are superfluous, because the females develop
parthenogenetically. A triploid female produces a triploid egg through mitosis,
which undergoes complete development without being fertilised. Haploid
males too develop parthenogenetically in the similar manner.

7.3.5 The Compound Chromosome System

Although the X is most commonly found as a single chromosome or single
homologous pair or chromosomes, some species have another variation –
compound chromosomes. These are named so because a group of
chromosomes (e.g. 8X, 12X, 6Y etc.), at the time of meiosis unite end to end
and behave as single unit. In such species, there are large differences in the
number of chromosomes in males and females. For example, in the nematode
Ascaris incurva there are 8X chromosomes and 1Y. This species has 26
autosomes. The diploid number of chromosomes in males is 35 (i.e., 26A + 8X
+ Y), and in females is 42 (or 26A 4- 16X).

In the above example, X chromosomes exist as a compound chromosome.

There are instances where both, the Y chromosomes and the X chromosomes
form compound groups., One such example is of Blaps polychresta, where the
male has 12x3 and 6Y's in addition to 18 autosomes..

7.3.6 The Transfer Gene

One additional complicating factor in sex determination in Drosophila is worth
examining briefly. This shows that the sex chromosomes (X and Y, Z and W)
are not the only ones involved in sex determination, but in addition numerous
autosomal genes also come into play. In Drosophila a recessive allele, tra, on
the third chromosome (an autosome), when homozygous, “transforms” normal
diploid females (AAXX) into sterile males. The tra gene has no effect in
heterozygous condition. The XX tra tra flies have many sex characters of
males (external genitalia, sex combs (see Fig. 7.6), and male type abdomen),
but are sterile. So are XXY tra tra flies. The XY tra tra males, however, are
normal and fertile.

Fig. 7.6: Drosophila melanogaster, (a) male, (b) female. Two distinguishing
features are: the merging of the posterior bands in the male versus
their distinct separation in the female, and the longer more tapering
abdomen of the female. (c) shows details of a male leg with sex comb
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(arrow).
Unit 7 Sex Determination
7.4 THE CHROMOSOME TNEORY OF
INHERITANCE AND SEX-LINKAGE
Soon after the discovery of Mendel's work in 1900, most geneticists accepted
the particulate nature of genes. Mendel had predicted that each gamete
contains only one allele of each gene instead of two. This prediction was
based on the fact this there is reduction in the number of chromosomes by
one-half at the time of meiosis during gamete formation.

This notion, that chromosomes carry genes is the Chromosome Theory of

Inheritance. The credit for the Chromosome Theory of Inheritance goes to
Walter Sutton and Theodor Boveri. In 1902, these investigators independently
recognized that the behaviour of Mendel’s genes during production of gametes
in peas precisely paralleled the behaviour of chromosomes at meiosis. The
following parallels were drawn between the two: i) genes are in pairs, so are
the chromosomes, ii) the members of gene pair segregate equally into
gametes, so do the members of a pair of homologous chromosome, and iii)
the different gene pairs act independently, so do the different chromosome
pairs.

The proposition of the Chromosome Theory was a crucial new step in genetic
thinking at that time. No longer were genes just disembodied factors, now they
were a part of the observable entities in the cell nucleus. Some geneticists,
particularly, Thomas Hunt Morgan remained skeptical of this idea. Ironically it
was Morgan himself who in 1910 provided the first definitive evidence for the
Chromosome Theory based on his studies on sex linkage.

Morgan worked with fruit fly Drosophila melanogaster. When he mated red-
eyed flies R II R (dominant) with white-eyed flies r r (recessive), the IF,
progeny were red-eyed. Furthermore, when Morgan mated red-eyed males of
the F, generation with their red-eyed sisters, they produced about 1/4 white-
eyed males, but no white-eyed females. In other words, the eye colour
phenotype is X-linked. X-chromosome and eye colour are transmitted together
because the genes governing this character are located on the X-
chromosome. In a diploid individual, we know, the autosomes occur in pairs
but as regards to X-chromosomes the female fly has two copies and the male
has just one. However, Morgan was reluctant to draw this conciusion until he
observed sex-linkage with two more characters - miniature wings and yellow
body in the fruit fly. That was enough to convince him and other geneticists of
the validity of the chromosome theory of inheritance.

7.5 SEX-LINKED INHERITANCE

The inheritance of genes located on the sex chromosomes follows a
characteristic pattern which is different from those located on the autosomes.
Here, we are elaborating on the XX-XY system as it pertains to man and most
of the examples cited are aim of human context. 189
Block 2 The Physical Basis of Heredity
7.5.1 X-Linked Traits in Humans
Let us first examine traits determined by genes on the X-chromosome, or the
X-linked traits. The human X chromosome contains many genes that are
required in both the sexes, whereas the Y chromosome contains only a few
genes, principally the genes for maleness. More than two hundred traits have
been found to be X-linked and only a few are known to be Y-linked. The traits
controlled by genes located on the X-chromosome are also referred to as sex-
linked. That is, the terms X-linked and sex-linked are used synonymously. It is
more appropriate, however, to refer to these as X-linked traits, since they
follow the pattern of transmission of the X-chromosome.

The X-linked traits have a unique mode of inheritance because females have
two doses of X-linked genes, while males have only one. Males are thus
hemizygous for X-linked traits.

X-Linked Dominant Genes

Dominant X-linked genes are always expressed in both the sexes just as
in autosomal traits. One dose of X-linked dominant allele produces its effects
in males as well as females. The hemizygous male transmits the gene to all its
daughters but none to his sons. There is no father to son transmission. The
heterozygous females transmit the trait to half their children, irrespective of
their sex. On the other hand, females homozygous for the dominant allele
produce all affected children. For example, a form of vitamin D-resistant
rickets is inherited as an X-linked dominant trait (Fig. 7.7).

Fig. 7.7: Pedigree demonstrating X-linked dominant trait. The affected progeny
are shaded.

X-Linked Recessive Genes

The opposite is true for recessive alleles. Males being hemizygous, always
express the recessive X-linked alleles. Females, however, express recessive
alleles only when they are homozygous. Thus, the frequency of X-linked
recessive traits is always lower in females than males.

Most X-linked genes are recessive alleles, and they are discovered when their
deleterious effects appear in males. Males transmit their X chromosome to
every daughter, and their Y chromosome to every son. Recessive X-linked
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traits thus show a pattern of inheritance, in which the phenotype is usually
Unit 7 Sex Determination
expressed only in males of alternate generations. A male bearer transmits the
recessive allele to daughters, who does not express the allele because it
occurs in the heterozygous condition. However, each of her male offspring has
a 50% chance of receiving that allele and expressing the phenotype. The trait
should thus appear in 1/4 of her offspring (1/2 of her offspring are expected to
be male and 1/2 of her sons receive the recessive allele: 1/2 × 1/2 = 1/4). The
heterozygous female is a carrier of the allele. The X-linked allele is often said
to show a criss cross pattern of inheritance. In this pattern of inheritance, the
allele is transmitted from male to female, female to male, and the trait is
expressed only in males in alternate generations (see Fig. 7.8). Well-known
examples of X-linked recessive alleles include Red green colour blindness,
Haemophilia, Glucose-6-phosphate dehydrogenase deficiency (G-6PD),
Congenital hyperuricemia, Duchenne muscular dystrophy, and Ichthyosis.

Fig. 7.8: Criss cross inheritance, i.e., the inheritance of a character from father
to daughter grandson. It is characteristic of a sex-linked gene. Genes
are shown on the chromosomes illustrating a cross between a woman
with normal vision and a green-colour defective man. The symbol g
represents the sex-linked recessive gene for green colour defective
vision, and G the normal condition. 191
Block 2 The Physical Basis of Heredity

SAQ 1
A husband and wife are normal although both their fathers have a trait which is
X-linked recessive. What is the probability that their first child will be:

a) A normal son?

b) a normal daughter?

c) a son with the trait?

d) a daughter with the trait?

Red Green Colour Blindness: Many persons cannot perceive certain

colours. The most common such defect is an inability to distinguish red from
green. This condition is also called partial colour blindness. Colour
perception is controlled by the cone-shaped cells in the retina of the eye.
Three types of cone cells, each containing a specific light absorbing pigment
(whose nature is protein), that perceives a specific portion of the visible
spectrum (see Fig. 7.9) have been identified. These three types of cone cells
are referred to as red-absorbing, green-absorbing and blue-absorbing cone
cells.

Fig. 7.9: Absorption spectra of the blue, green and red proteins present in the
cone cells of the retina of the human eye. The ability of humans with
normal colour vision to distinguish colours throughout the visible
spectrum depends on the presence of all three proteins. Defective
colour vision results from the absence of, or a defect in, one or more of
these proteins. [After Nathans, K 1989. The Genes for: colour vision, Sa.
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Amer, 260(2): 42-49].
Unit 7 Sex Determination
By 1986, the genes that encode the above three light-absorbing pigments of
the retina were isolated and their nucleotide sequence was determined. The
sequences have been used to find out the amino acid sequences of the three
light absorbing proteins. These light-absorbing proteins were found to have
very similar structures. The genes that encode the green-, and red-receptor
proteins are located on the X-chromosomes, thus the sex-linked patterns of
inheritance are observed for defects in green and red colour vision. And the
gene encoding the blue receptor protein was found to be located on
chromosome-7, that is, an autosome. Let us now examine some crosses (see
Fig. 7.10) and assess the pattern of inheritance of this defect. For the sake of
simplicity we are only considering here one gene, that is, gene causing defects
in the green receptor protein, as a single sex-linked recessive allele. Since the
Y chromosomes carried no colour vision locus, the single allele is expressed
causing colour blindness. Stop here for a minute and carefully study the five
crosses in the figure. The symbol G denotes normal receptor pigment, and g is
for the defective receptor pigment causing colour blindness.

Fig.7.10: Five possible crosses involving inheritance of sex-linked recessive

trait – partial colour blindness: a) normal male × colour blind female; b)
colour blind male × normal female; c) colour blind male × normal
female who is a carrier; d) normal male × normal female who is a
carrier; e) colour blind female × colour blind male.

In the above crosses have you noticed that sex-linked inheritance does not
conform to the Mendel’s laws of inheritance? Fig. 7.10 shows the results of
reciprocal matings of affected and unaffected parents. The normal male and
colour blind (recessive, homozygous) female produce normal but
heterozygous daughters, but all sons have the disease (cross a). The
reciprocal cross (b) demonstrates criss cross inheritance. A colour blind male
(hemizygous) with a normal (homozygous) female produces no affected
offspring, but the daughters are carriers (cross b). A colour blind male and a
carrier female result in 50% colour blinds (see cross c). Another possibility, a
normal male mated with a carrier female, produces all normal, female offspring
but 50% affected male offspring (see cross d). The mating of two colour blind
individuals result in all colour blind offspring (see cross e) if they have the
same colour blindness. 193
Block 2 The Physical Basis of Heredity
Haemophilia: Haemophilia is a disease in which one of the factors required
for the normal clotting of blood (see Fig. 7.11) is deficient. As a result, the
blood fails to clot or clots very slowly. Thus even minor injuries can cause
profuse internal and external bleeding which can lead to death.

Fig. 7.11: Blood clotting is the end result of a series of reactions requiring
various enzymes and cofactors, leading to the formation insoluble
fibrin. Many of the steps in the chain entail the conversion of a gene
Haemophilia is one of product to its active enzymatic lor111 by the enzymatic action of the
the earliest known active product a previous step. Cofactors (e.g., factor VIII and V) are
diseases, According required to work along with some of the active enzymes. Factor VIII,
to Talmud, the absent/defective in haemophilia A, is a cofactor required along with
Hebrew book of law, factor 1X to activate factor X. If factor VII is absent as a result of a sex-
when excessive linked recessive condition, the sequence is interrupted and the end
bleeding occurred result is defective clotting. In haemophilia B, factor a is deficient.
during circumcision of
two male infants of a Three forms of haemophilia controlled by three different gene loci are known.
mother, future male One of them is rare and is controlled by an autosomal recessive gene, while
offspring were
two forms, that is, haemophilia A and B result from recessive alleles at two X-
exempt. When sons
of three sisters linked loci. Haemophilia B also known as Christmas disease, comprises about
exhibited bleeding, 20% of all haemophilia and is caused by the deficiency of factor IX (see Fig.
sons of other sisters 4.7, step 3).
were also exempt.
However, sons of Haemophilia A, classical haemophilia is caused by an abnormality or
brothers were not deficiency of a protein cofactor known as factor VIII is located on X-
exempt, implying an chromosome. Factor VIII is needed for the activity of one of the enzymes -
understanding of criss factor IX, in the series of events leading to the activation of thrombin. Absence
cross pattern of
of functional factor VIII interrupts the steps leading to the activation of
inheritance.
thrombin, and consequently fibrin cannot form. Until recently, haemophilia A
was untreatable and only about 25% of the affected males reached age of
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twenty five. Treatment with factor VIII now results in a longer life span.
Unit 7 Sex Determination
The frequency of haemophiliacs is about one in ten thousand males, but is
much lower in females, about one in one hundred million or less. A female
haemophiliac can result from the mating of a heterozygous female with an
affected male. Such a mating, is highly unlikely because very few male
haemophiliacs survive long enough to reproduce. Haemophiliac females are
also belived to die at the onset of menstruation.

Haemophilia A has been called the “Royal disease” because it affected males
in the royal families of Europe. Queen Victoria, a carrier of the haemoptrilia
allele had nine children (Fig. 7.12). Her eighth child, Leopold was a
haemophiliac who died at the age of thirty one. Her other three sons were
unaffected as they did not receive the allele. One daughter had no children,
her status as a carroerr cannot be assessed. Two daughters had children,
none of whom were haemophiliac, indicating that mothers probably were not
carriers. Two other daughters were carriers giving birth to haemophiliac sons.

The possible historical influence of haemophilia is tentalising. Victoria’s third

child was princess Alice, whose daughter Alexandra married Czar Nicholas II
of Russia. The Czarina, Alexandra, had four daughters before giving birth to
the long awaited son Alexis - the heir to the Russian throne. Unfortunately,
Alexis had the haemophilia allele, a legacy from his great grandmother –
Queen Victoria. Distressed over their son's condition, the Czar and Czarina
turned to the monk Rasputin. While affairs of the state deteriorated,
culminating in Russian revolution, the Czar was preoccupied with the health of
his son.

Among Victoria’s descendants, eight of twenty five males in four generations

were haemophiliacs. Queen Victoria almost certainly received the gene for
haemophilia A, as a result of mutation on the X chromosome which she
received from her father Edward, Duke of Kent. He was fifty-two years old at
the time of Victoria's birth and such mutations may occur more frequently in
the germ cells of older males.

In the recent years, a serious threat to victims of haemophilia has arisen due
to their continuing dependence upon blood transfusions. Such transfusions are
one means of transferring Acquired Immune Deficiency Syndrome (AIDS)
and some haemophiliacs have infact acquired AIDS in this way. Extensive
surveillance of donor blood supplies is required to protect haemophiliacs and
all others requiring transfusions.

Glucose 6-Phosphate Dehydrogenasc (G-6PD) Deficiency: Another

disease due to defective X-linked recessive allele is G-6PD. This is an
important enzyme, for carbohydrate metabolism and maintaining stability of
red blood cells.

Deficiency of enzyme G-6PD is a rare condition characterised by severe

haemolytic anaemia (due to destruction of red blood cells) when exposed to
environmental triggers such as fava beans, naphthalene and certain sulpha
drugs. 195
Block 2 The Physical Basis of Heredity
Congential Hyperuricemia – Lesch-Nyhan Syndrome: This disease is
characterized by the excess production of uric acid. A mother contributes the
X-chromosome with defective gene to a male zygote. Half of the male children
of carrier mothers may be expected to inherit the disease. They are deficient
for the enzyme hypoxanthine-guanine phosphoribosyl transferase (HGPK’T).
This enzyme is involved in nucleotide synthesis. Infants who receive the gene
appear normal at birth. The initial symptom of the disease is the production of
excessive uric acid in the urine as a result it appears as orange sand-coloured.
By 10 months of age, the patients become abnormally irritable and lose motor
control. Weak and flabby muscles prevent the child from sitting, walking and
speaking normally. As the disease advances, there is deterioration of nervous
system. Self-mutilation occurs, manifested by lip-biting, finger-chewing, teeth-
grinding, and marked swinging of the arms. Eventually death occurs within a
few years due to severe renal and neurological damage. Some of the patients
live to their twenties.

Duchenne Muscular Dystrophy (DMD): It is another example of an X-linked

recessive allele, that primarily affects young males. Half of tile male progeny of
a carrier female are expected to be affected. In the affected males
deterioration begins between the ages of three and five years, but sometimes
the affected individuals reach their teens. But they are confined to wheel
chairs; and they die in their early twenties due to atrophy of their respiratory
muscles. Only few affected males reproduce, so the condition transmitted
mainly by female carriers. This disease occurs in about one in every four
hundred newborn males; and is several times more frequent then haemophilia.
In 1986, the defective gene that causes DMD was isolated and studied. It was
found that the absence or a protein – dystrophin caused DMD.

Ichthyosis: So far you have seen the examples where the recessive X-linked
are expressed in males. There are, however, instances where these are also
expressed in females in certain situations. Consanguineous matings (see
Consanguineous
means “of the same adjacent Margin Remark) can greatly increase the frequency of expression of
blood”. The term X-linked traits in females. In consanguineous pedigrees containing X-linked
means sharing genes recessive alleles, females have a high probability of carrying the X-linked
derived from a allele, as they can receive the allele from either parent. In turn, matings of
common ancestor, carrier females and affected males (Fig. 7.12) produce daughters and sons
related by descent. with an equal likelihood (i.e., 50%) of being affected.

Fig. 7.12: Cross between ichthyosis carrier female and affected male showing
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50% affected progeny.
Unit 7 Sex Determination
Ichthyosis is a disorder characterised by extreme dryness, roughness and
scaliness of the skin. The prefix ‘ichthy’ means fish-like. Children produced in
situation as shown in Fig. 7.12 show ichthyosis at birth.

SAQ 2
A couple have a colour blind daughter and son with normal vision. What are
the genotypes of the parent in this cross?

SAQ 3
Draw a three generation pedigree of a family starting from a couple, where
male is a haemophiliac and the female is normal. They have 3 sons and a
carrier daughter. The daughter marries a normal male and has 3 daughters
and 2 sons. What is the probability of her children being carriers and
haemophiliacs?

7.5.2 Y-Linked Traits in Humans

Any gene that occurs exclusively on the Y chromosome is said to be

holandric and it is not expressed in females. Such a Y-linked gene normally
occurs in males and is transmitted only from father to son – holandric
inheritance. Only a few Y-linked genes have been identified uptil now. One is
the histocompatibility gene, known as the H-Y gene which is present on the
short arm of the Y chromosome. Another important Y-linked gene is the TDF
gene that codes for testis determining factor. This locus plays an important
role in primary sex determination. The functional significance of TDF gene
would be explained in Unit 5.

Another phenotype known to be associated with the Y chromosome is the

condition hypertrichosis. The gene concerned with this condition leads to the Fig. 7.13: Hen-
development of hairy pinna (Fig. 7.13). This phenotype has been observed ill feathering (top), and
the inhabitants of Australia, Ceylon, Israel, and India. cock-feathering
(bottom) in domestic
fowl.
SAQ 4
A man has hypertrichosis of the ears, a condition due to a gene on the Y-
chromosome. Show the types of male and female children he has.

SAQ 5
Is a Y-chromosome linked gene supposed to be dominant or recessive in
order to be recognised? How is a Y-linked gene transmitted to grand children?
197
Block 2 The Physical Basis of Heredity
7.6 SEX-LIMITED AND SEX-ENFLUENCED
TRAITS
Not all of the characters that differ in the two sexes are X-linked. There are
certain traits that are determined by autosomal genes, but their expression is
altered or influenced by the sex of the individual. Many a times these traits are
confused with the sex-linked traits. Actually, they are entirely different in their
mode of inheritance since their genetic determinants are not located on the
sex chromosomes. There are two kinds of such traits: sex-limited, and sex-
influenced traits.

7.6.1 Sex-Limited Traits

Sex-Limited Traits are traits expressed only in one sex, although the genes
controlling them are present as well as transmitted to both the sexes.
Therefore, males and females with the same genotype, with respect to a
particular locus may have different phenotypes.

Sex-Limited Traits are determined by autosomal genes, whose phenotypic

expression is determined by the presence or absence of one of the sex
hormones. Since sex hormones are the limiting factors, the phenotypic
expression of these genes is limited to one sex or the other. The most obvious
examples are the secondary sex characteristics. Beard development in human
beings is one such sex-limited character as men have beards, and woman
normally do not. Yet studies indicate no significant differences between the
sexes in number of hairs per unit area of skin surface except in their
development. This appears to depend on sex hormone production. Any
disturbance in these hormones in women may result in the development of
beard. Similarly, [he full development of breasts in females, and presence of
prostate glands in males are the examples of sex-limited traits seen in human
beings. Traits like egg laying in chickens, oviposition behaviour in insects are
some other such examples. Milk production in mammals is limited to females,
but certain bulls are in great demand among dairy breeders and artificial
insemination associations because their mothers and daughters have
increased milk production records.

Another classic example of a sex-limited trait is “cock feathering” in different

birds. We consider here the example of domestic fowl, the males and females
exhibit pronounced difference in their plumage. In the leghorn breed the males
have long, pointed, curved, fringed feathers on tail and neck, but feathers on
females are shorter, rounded, straighter, and without fringe (see Fig. 7.14).
Fig. 7.14: Pattern-
Thus males are cock-feathered and females are hen-feathered. In the breeds
baldness in man.
Sebright bantam, birds of both sexes are hen-feathered. However, in Hamburg
and Wyandotte, both hen-, and cock-feathered males are seen, but all the
females are hen-feathered. The feathering type depends on a single pair of
198
36
alleles Hand h in the following manner (Table 7.1).
Unit 7 Sex Determination
Table 7.1: The Feathering Type in Domestic Fowl.

Genotype Male Female

HH hen-feathered hen-feathered

Hh hen-feathered hen-feathered

hh hen-feathered cock-feathered

Thus Sebright bantams are all HH. Hamburgs and Wyandottes may be H-, or Pattern baldness
hh, and Leghorns are all hh. Cock-feathering where it occurs is limited to the refers to a definite
male sex. genetic pattern. In
this condition hair
7.6.2 Sex-Influenced Traits usually thins on top
ultimately leaving a
Sex-Influenced or Sex-Controlled Traits appear in both sexes but occur in fringe of hair low on
one sex more than the other. the head (Fig. 4.13).
Baldness may also
The genes for Sex-Influenced Traits show differing patterns of expression in arise due to various
each sex-usually the trait behaves as dominant in one sex and a recessive in causes such as
the other. Genes for sex-influenced traits occur only on autosomes. disease, radiation,
thyroid defect.
The best documented example of sex-influenced inheritance is pattern
baldness (Figs. 7.15 and 7.16). Individuals expressing pattern baldness begin
to lose their hair on the front and the top of the head, relatively early in life,
often in their twenties. Affected individuals are not totally bald: a distinct rim of
hair surrounds their head in patterns varying from person to person. It has
been proposed that a single pair of alleles is involved. The allele B1 which is
responsible for pattern baldness is dominant in males, and the heterozygous
males therefore, express pattern baldness. In females, however, the gene is
recessive. The allele for normal hair growth can be designated as B2.
Individuals with the genotype B1 B1 show pattern baldness, regardless of sex.
In such situations, in females there is marked thinning, rather than total loss of
hair on the top of the head. Persons with B1B2 genotype ale bald if they are
male but not bald if they are female. The presence of male hormones, are
strongly implicated in the expression of pattern baldness.

Fig. 7.15: Pedigree showing the incidence of pattern, baldness in a family. The
men represented by the dark squares became bald before they
reached the age of 35. Those represented by light squares are over 35
and have thick hair. No woman in this family pedigree expressed the
trait (After Gardner el ul. 1991, Principle of Genetics, John Wile-y h
Sons, Inc.) 199
Block 2 The Physical Basis of Heredity
Some human traits, such as certain types of white forelock, absence of upper
lateral incisor teeth, a particular type of enlargement of the terminal joints of
the fingers, and cleft-lip, exhibit a pattern of inheritance characteristic of sex-
influenced genes.

A few well-known examples of sex-influenced genes in animals are: spotting in

cattle (mahogany and white dominant in mares, red and white dominant in
females), horned versus hornless condition in sheep (Fig. 7.16) where the
autosomal gene involved is dominant in males and recessive in females.

Fig. 7.16: Rocky mountain sheep showing sexual dimorphism in horn

development. The male has large horns, whereas the female is devoid
of them.

SAQ 6
Compare the inheritance pattern of the sex-limited traits with those of the sex-
linked traits.

7.7 DOSAGE COMPENSATION

Recall that in the XX-XY chromosome system, males have only one X
chromosome (hemizygous) while the females have two. Thus the males have
half the number of X-linked genes as females. In other words, the males have
only one dose of X chromosomes and the females have double dose of X-
chromosomes. We know that the amount of gene product in cells is related to
the number of gene copies present, it would be expected that females would
have double the amount of X-linked gene products as compared to males.
Now the question arises, is there any compensation for this dosage difference
between sexes? The answer is ‘Yes’, there is a mechanism which regulates
the levels of gene products in such a way that both hemizygous and
heterozygous/homozygous individuals that is, males and females, have
the same amount of gene product. This mechanism is known as Dosage
200
36
Compensation.
Unit 7 Sex Determination
7.7.1 In Man
In human and other mammals, the necessary dosage compensation is
accompanied by inactivation or “turning off” of one of the X chromosomes
in females so that both males and females have only one functional X
chromosome per cell. The inactive X chromosome, in females becomes tightly
coiled into ‘heterochromatin’ a condensed form of chromatin visible as a dark
spot – X-chromatin or Barr body (after its discoverer M.L. Ban) in the
nucleus of female cell (Fig. 7.17.). Thus Barr body is the inactivated X
chromosome. One X chromosome is necessary for normal development in
both sexes, but if an individual (or either sex) has more than one X- Fig. 7.17: Barr Body
chromosomes, all but one are inactivated and are visible in stained somatic in the nucleus of a
cells as Barr bodies. Thus somatic cell nuclei of normal males have no Barr cell of a normal
body, and those of normal females have one (also see Box 7.1). female.

Box 7.1: Detection of Barr Body

A simple-way to demonstrate the Barr Body in humans is by scraping

epithelial cells from the buccal mucosa of females, and staining them
with a specific dye. The nuclei in many cells would show a small,
diamond-shaped structure about 1 µm in diameter, more deeply stained
than the surrounding chromatin and usually located at the periphery of
the nucleus. This body stains positively in the Feulgen reaction for
DNA.

The hypothesis that all but one X chromosome(s) are inactivated in each cell
was proposed by the geneticist Mary F. Lyon in 1961 and is known as Lyon
hypothesis. Crucial evidence for this hypothesis was provided by sexually
aneuploid individuals. Aneuploidy (meaning not the true number) refers to the
possession of an abnormal number of chromosomes. Aneuploid individuals
have the normal diploid number, plus or minus one or more chromosomes.
Females lacking one X chromosome exhibit Turner’s syndrome, designated
45, XO (45 chromosomes, with one X missing). Males with an extra X-
chromosome have Klinefelter’s syndrome designated 47 XXY. Cells from
45, XO females and 46 XY males have no Barr bodies (Fig. 7.18 a); while
those from 47, XXX females and 48 XXXY males have two (Fig. 7.18 b); 46,
XX females and 47, XXY males have one Barr body (Fig. 7.18 c) and 48,
XXXX females and 49, XXXXY males have three Barr bodies (Fig. 7.18 d).
Examination of the number of Barr bodies can be done easily to screen for
sex-chromosomes abnormalities. You have already seen in Box 7.1 how to
make a preparation of the epithelial cells from the buccal cavity for
examination. The mandatory "sex test\" that have been required for Olympic
athletes includes a count of Barr bodies. Males disguised as females can be
identified as they have no Barr bodies.

The inactivation of X chromosomes during development occurs at random.

Early in development, the maternally derived X is inactivated or Iyonised in
some, while the paternally-derived X is inactivated in others. Thereafter,
descendants of a particular cell have the same X inactivated (Fig. 7.19). If a
female is heterozygous for an X-linked gene, she is mosaic for that trait. One
of her X-chromosomes is active in roughly half of her cells while the second X
is active in other cells. That is to say that some cells express X-linked genes
inherited from the father while others express those passed on by the mother. 201
Block 2 The Physical Basis of Heredity

Fig. 7.18: Diagrammatic representation of varying number of Barr bodies in

different genetic make ups.

Fig. 7.19: Diagrammatic representation of the random inactivation of one of the

two chromosomes in female cells, all progeny cells inactivate the
same chromosome. All descendants of these cells have the same
chromosome inactivated, so females are mosaics for their maternally-
derived and paternally-derived X chromosomes.

Calico cats (Fig. 7.20) exhibit mosaicism, due to dosage compensation.

Several loci control coat colour in cats, but only one X-linked locus is involved
in producing calico individuals. Two alleles occur at that locus, R and R: In
males (hemizygous), R produces rust coat colour and R black. In females R
inactivation produces clones of R-bearing rust fur intermixed with R-bearing
black fur – the calico cat. Thus almost all calico cats are females. Male calico
cats, only result because of sex-chromosome aneuplioidy. XXY males also
202
36
undergo X inactivation, so an occasional calico male is seen.
Unit 7 Sex Determination
When a female is heterozygous for a deleterious X-linked allele, the effects of
the cell lines bearing the normal allele may compensate for the harmful effects
of the cell lines bearing the deleterious allele. In females heterozygous for
partial colour blindness, for examples, some cell clones in the retina are in fact
colour blind, hut the presence of other normal clones results in normal colour
vision.

Another example that shows the genetic consequences of X-inactivation in

females heterozygous for an X-linked gene is the enzyme G-6PD. Cell
cultures from an individual heterozygous for the G-6PD gene, has alleles with Fig. 7.20: A calico cat
two forms of the enzyme: G-(IPD type A ant1 G-6PD type B. In spite of the with patches of colour
cells carrying both the alleles, half the cells express G-6PD type A enzyme, resulting from random
inactivation of X
while the remaining express C;-6PD type B enzyme. If one cell from this
chromosomes bearing
culture was made to grow in isolation then all cells arising from it express the colour determining
same enzyme type as its parent cell. It confirms the hypothesis that X- genes in cells giving
inactivation is clonally transmitted, i.e., the same inactivated X-chromosome is rise to hair.
passed to daughter cells throughout repeated cell divisions.

The inactivation of one of the two X chromosomes in females must be

reversible, since females transmit both of their X chromosomes to their
progeny in a functional state. This is especially clear in the case of
hemizygous male progeny which receives either of the X chromosome of the
mother with equal probability, because the single X chromosome that each
son receives must be fully active given that the X chromosomes contains
many genes that are vital to the growth and development, indeed to the
survival. The reactivation-“turning on” of the inactive heterochromatic X
chromosomes of mammalian females occurs in germ cell lineages prior to
oogenesis. Both X chromosomes of a female are active in the oogonial cells.

The maintenance of the germ cells and ovarian structures requires the
presence of two X-chromosomes. At this point you may wonder, whether
normal reactivation ever fails to occur. There are considerable evidences that
indicate abnormal reactivation of the heterochromatic X chromosomes. The
most common form of inherited mental retardation in humans is its example.

7.7.2 In Drosophila

Dosage compensation occurs in fruit flies, but its mechanism is different from
those of the mammals. No barr bodies are found in fruit flies. You have
already learnt that in fruit flies, the X chromosome to autosome ratio is
responsible for sex determination. Normal females have two X chromosomes
and normal males have one X chromosome. Dosage compensation in this
case is achieved by increased transcriptional activity of genes on the single X
chromosome in male cells relative to that of each of the X chromosome in
female cells The male has hyperactive X-chromosome, approaching the level
of activity of both of the females. This hyperactivity of X-chromosome can be
cytologically seen as “puffed” bands in the salivary gland chromosomes (Fig.
7.21). This is in variance to the inactive X-chromosomes in mammals which
appears condensed (sex chromation body). 203
Block 2 The Physical Basis of Heredity

Fig. 7.21: a) The salivary gland chromosomes of Drosophila melanogaster. b) A

portion of the puffed band enlarged.

SAQ 7
Indicate the expected number of Barr bodies in interphase cells of the
following individuals: Klinefelter’s syndrome; Turner’s syndrome; and
Karyotypes 47 XYY, 47 XXX, and 48 XXXX.

SAQ 8
Cat breeders are aware that kittens with the calico coat pattern are invariably
females. Why?

7.8 SUMMARY
In this unit you have learnt that:

• The chromosomes are the carriers of genes and the transmission of

chromosomes from one generation to the next closely parallels that of
the genes.

• In species with an XX-XY mechanism, genes on the sex chromosomes

may be X-linked or Y-linked.

• The mode of transmission of sex-linked traits is different from that of the

autosomal ones.

• The dominant X-linked traits are always expressed in both the sexes.

• Recessive X-linked traits show a criss-cross pattern of inheritance.

Female heterozygotes are carriers who pass the trait to 50% of their
male offspring. Recessive X-linked traits are expressed far less
204
36
commonly in females than in males.
Unit 7 Sex Determination
• Only a few Y-linked genes have been identified and amongst them TDF
(Testis determining factor) plays a role in male sex determination.

• Sex-limited and sex-influenced traits are the result of genes on the

autosomes. The expression of these genes is sexually dimorphic.

• Dosage compensation regulates the level of gene products in such a

way that both males and females have the same amount of gene
products.

• In female mammals including man, dosage compensation occurs by the

inactivation of all the X-chromosomes except one (forming Barr body or
bodies) whereas in fruit flies it occurs by the hyperactivation of the single
X-chromosome in males.

7.9 TERMINAL QUESTIONS

1. List at least four criteria for identifying X-linked recessive traits from
pedigree studies.

2. Choose the correct answer.

i) Which one of the following statements does not apply to human

sex chromosome?

a) carry allelic pairs

b) determine individual sex

c) are identical in women

d) are identical in man

e) both a and d

ii) Barr bodies result from:

a) inactivation of one X chromosome by the Y chromosome

b) a third X chromosome

c) inactivation of one X chromosome for dosage compensation

d) both b and c

iii) A man and a woman are both affected by vitamin D-resistant

rickets which is a dominant sex-linked allele. All of the female
offspring of these people are affected with rickets, but some of the
males are not. What are the possible genotypes of the parents?

a) both are homozygous for the trait

b) the woman is heterozygous for the trait

c) the woman is homozygous and the man is heterozygous

d) this is not possible. 205

Block 2 The Physical Basis of Heredity
iv) The fly Drosophila melanogaster has a gene that codes for white
eyes as recessive and X-linked. Red eyes result from the wild type
allele at the same locus. A cross between a heterozygous red-
eyed female and white-eyed male would produce:

a) all red-eyed progeny

b) all white-eyed males and all-eyed females

c) one red-eyed male and one white-eyed male

d) one red-eyed female and one white-eyed female

e) both c and d

v) The gene for pattern baldness is dominant in men, but exhibits

recessiveness in women. The difference in expression results
from:

a) the gene for baldness being X-linked

b) the gene for baldness being Y-linked

c) the expression of the gene depending upon the hormonal

balance of the individual

d) both a and c

e) none of the above

3. Fill in the blanks:

i) Men have ----------------- pairs of autosomes and one -----------------

pair of sex chromosomes.

ii) Women have ---------------- pairs of autosomes and one ---------------

pair of sex chromosomes.

iii) The fertilization of an egg by a Y sperm results in a -----------------

offspring.

iv) Genes which are Y-linked are called -----------------.

v) Sex-limited genes are those whose phenotypic expression is

determined by the presence or absence of sex -----------------.

vi) Beard development in humans is generally limited to one sex

(male), yet studies indicate that there is no real difference in the
number of hairs per unit area of skin between men and women.
This indicates that beard development is a ----------------- trait.

4. Match the terms in column A with their appropriate descriptions in

column B:

Column A Column B

i) Dosage compensation a) X-chromatin

ii) Turner’s syndrome b) inactivation of one X chromosome

206
36
Unit 7 Sex Determination
iii) Klinefelter’s syndrome c) inactivation of one X chromosome
so as to reduce to half the allele

iv) Barr body d) inactivation of all but one X

chromosomes

v) Lyon hypothesis e) phenotypically female (XO)

f) phenotypically male (XXY)

5. In sheep, the gene h+ for the horned condition is dominant in males and
recessive in females. If a hornless ram were mated to a horned ewe,
what is the chance that:

a) an F2 male sheep will be horned or

b) an F2 female sheep will be horned?

6. In chicken, the gene h] which distinguishes hen-feathering from cock-

feathering, is sex-limited. Males may be hen-feathered or cock-
feathered, but female are always hen-feathered. If a cock-feathered
male (hh) were mated to a homozygous (h+h+) hen-feathered female,
what patterns of feathering might be expected among the (a) male F2
and (b) female F2 progeny?

7. In Drosophila, the gene for bobbed bristles (recessive allele bb, bobbed
bristles; wild-type allele bb+, normal bristles) is located on the X
chromosomes and on a homologous segment of the Y chromosome.
Give the genotypes and phenotypes of the offspring from the following
crosses: a) XbbXbb × XbbYbb+, b) XbbXbb × XbbYbb, c) Xbb+Ybb, d) Xbb+Xbb ×
XbbYbb+.

8. Make a diagram for a cross between a normal woman (whose father was
defective in green colour vision) and a green colour-defective man.
Summarise the expected for sex and colour vision.

7.10 ANSWERS
Self Assessment Questions
1. Since both the husband and wife have fathers with the X-linked trait, the
husband will not carry the trait as it receives its X-chromosome from his
mother, but the wife carries the trait as she gets one X-chromosome
from her father. a) The probability of having a normal son is fifty per cent.
b) The chances of having a normal daughter is hundred per cent as a
female is not affected with X-linked recessive trait unless she receives
two genes for the trait. c) There is fifty per cent probability of having
affected son. d) There is no chance of the daughter being affected, but
there is a fifty per cent probability that they may be carrier.

2. Since the daughter is colour blind it can be assumed that both parents
carry the genes for the trait. The father’s genotype is therefore,
hemizygous and that of the mother is heterozygous for the trait. The son
must have received the normal X-chromosome from the mother and is
therefore, normal. 207
Block 2 The Physical Basis of Heredity
3.

The probability is fifty per cent for the daughters being carriers and there
is fifty per cent probability of the son being a haemophiliac.

4. Only the male children have hypertrichosis ear as the gene or it is Y-

linked and the Y is passed from father to son. Females don’t have the
trait as they never posses a Y-chromosome.

5. Irrespective of whether a Y-linked gene is recessive or dominant it can

be recognized as it is always present in hemizygous condition. The Y-
linked gene is transmitted from grandfather to male grand-children
through the father. The female grand-children are unaffected so are the
daughters and the grand-children born from them.

6. Sex-linked inheritance patterns are quite different from those of sex-

limited ones. The latter may be expressed in either sex, though with
differential frequency. Genes for sex-limited traits express their effects in
only one sex or the other and their action is clearly related to sex
hormones. They are principally responsible for secondary sex
characters.

7. Klinefelter-one; Turner-none; 47 XYY-none; 47 XXX-two; 48 XXXX

three.

8. Because the mosaic coat pattern is due to the expression of sex-linked

heterozygous alleles according to the Lyon hypothesis.

Terminal Questions
1. i) The trait occurs more frequently in males than in females.

ii) Traits are transmitted from an affected man through his carrier
daughters to half his grandsons.

iii) An X-linked allele is never transmitted directly from father to son.

iv) All affected females have an affected father and a carrier or

affected mother.

2. i) e, ii) c, iii) b, iv) e, v) c.

3. i) 22, XY, ii) 22, XX, iii) male, iv) holandric, v) hormones,
208
36
vi) sex-limited.
Unit 7 Sex Determination
4. i) b, ii) e, iii) f, iv) a, v) d.

5. a) 3/4, b) 1/4.

6. a) 3 hen-feathered : 1 cock-feathered

b) All hen-feathered

7. a) 1/2 XbbXbb bobbed females, 1/2 XbbYbb+ wild males;

b) 1/2 XbbXbb+ wild females, 1/2 XbbYbb bobbed males;

c) 1/2 XbbXbb+ and XbbXbb+ wild females, 1/4 Xbb+Ybb wild males, 1/4
XbbYbb bobbed males;

d) 1/4 Xbb+Xbb wild females, 1/4 XbbXbb bobbed females, 1/2 Xbb+Ybb+
and XbbYbb+ wild males.

8.

209