I 5.12 Pattern baldness is a sex-influenced trait. This trait is seen in three generations of the Adams family: (a) John Adams (1735-1826), the second president of the United States, was father to (b) John Quincy Adams (1767-1848), who was father to (c) Charles Francis Adams (1807-1886). Pattern baldness results from an autosomal gene that is thought to be dominant in males and recessive in females. (Part (a) National Museum of American Art, Washington, D.C./Art Resource, NY; (b) National Portrait Gallery, Washington, D.C./Art Resource, N.Y.; (c) Bettmann/Corbis.)
separate into gametes according to Mendel's principle of segregation, and all the Fj are heterozygous (B+Bb). Because the trait is dominant in males and recessive in females, all the Fj males will be bearded, and all the Fj females will be beardless. When the Fj are crossed with one another, J/4 of the F2 progeny are BbBb, J/2 are BbB+, and J/4 are B+B+ (< Figure 5.11b). Because male heterozygotes are bearded, 3/4 of the males in the F2 possess beards; because female heterozygotes are beardless, only j/4 of the females in F2 are bearded.
An example of a sex-influenced characteristic in humans is pattern baldness, in which hair is lost prematurely from the front and the top of the head ( FIGURE 5.12). Pattern baldness is an autosomal character believed to be dominant in males and recessive in females, just like beards in goats. Contrary to a popular misconception, a man does not inherit pattern baldness from his mother's side of the family (which would be the case if the character were X linked, but it isn't). Pattern baldness is autosomal; men and women can inherit baldness from either their mothers or their fathers. Men require only a single allele for baldness to become bald, whereas women require two alle-les for baldness, and so pattern baldness is much more common among men. Furthermore, pattern baldness is expressed weakly in women; those with the trait usually have only a mild thinning of the hair, whereas men frequently lose all the hair on the top of the head. The expression of the allele for pattern baldness is clearly enhanced by the presence of male sex hormones; males who are castrated at an early age rarely become bald (but castration is not a recommended method for preventing baldness).
An extreme form of sex-influenced inheritance, a sex-limited characteristic is encoded by autosomal genes that are expressed in only one sex—the trait has zero penetrance in the other sex. In domestic chickens, some males display a plumage pattern called cock feathering ( FIGURE 5.13a). Other males and all females display a pattern called hen feathering ( FIGURE 5.13b and c). Cock feathering is an autosomal recessive trait that is sex limited to males. Because the trait is autosomal, the genotypes of males and females are the same, but the phenotypes produced by these genotypes differ in males and females:
HH Hh hh
Male phenotype hen feathering hen feathering cock feathering
Female phenotype hen feathering hen feathering hen feathering
An example of a sex-limited characteristic in humans is male-limited precocious puberty. There are several types of precocious puberty in humans, most of which are not genetic. Male-limited precocious puberty, however, results from an autosomal dominant allele (P) that is expressed only in males; females with the gene are normal in pheno-type. Males with precocious puberty undergo puberty at an early age, usually before the age of 4. At this time, the penis enlarges, the voice deepens, and pubic hair develops. There is no impairment of sexual function; affected males are fully fertile. Most are short as adults, because the long bones stop growing after puberty.
Because the trait is rare, affected males are usually heterozygous (Pp). A male with precocious puberty who mates
5.13 A sex-limited characteristic is encoded by autosomal genes that are expressed in only one sex. An example is cock feathering in chickens, an autosomal recessive trait that is limited to males. (a) Cock-feathered male. (b) and (c) Hen-feathered females. (Part a, Richard Kolar/Animals Animals; part b, Michael Bisceblie/Animals Animals; part c, R. OSF Dowling/Animals Animals.)
with a woman who has no family history of this condition will transmit the allele for precocious puberty to 1/2 of the children ( FIGURE 5.14a), but it will be expressed only in the sons. If one of the heterozygous daughters (Pp) mates with a male who has normal puberty (pp), / of the sons will exhibit precocious puberty ( FIGURE 5.14b). Thus a sex-limited characteristic can be inherited from either parent, although the trait appears in only one sex.
The results of molecular studies reveal that the underlying genetic defect in male-limited precocious puberty affects the receptor for luteinizing hormone (LH). This hormone normally attaches to receptors found on certain cells of the testes and stimulates these cells to produce testosterone. During normal puberty in males, high levels of LH stimulate the increased production of testosterone, which, in turn, stimulates the anatomical and physiological changes associated with puberty. The P allele for precocious puberty codes for a defective LH receptor, which stimulates testosterone production even in the absence of LH. Boys with this allele produce high levels of testosterone at an early age, when levels of LH are low. Defective LH receptors are also found in females who carry the precocious-puberty gene, but their presence does not result in precocious puberty, because additional hormones are required along with LH to induce puberty in girls.
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