In Drosophila subobscura, the presence of a recessive gene called grandchildless (gs) causes the offspring of homozygous females, but not those of homozygous males, to be sterile. Can you offer an explanation as to why females and not males are affected by the mutant gene?

Short Answer

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Short Answer: The recessive "grandchildless" gene affects the offspring of homozygous females but not males in Drosophila subobscura due to differences in their reproductive systems. The gene may negatively impact egg development in females, leading to sterility in their offspring, while leaving sperm development or function in males unaffected.

Step by step solution

01

Understanding recessive genes and their inheritance

The grandchildless gene is recessive, which means that it is only expressed when an individual has two copies of the gene (one from each parent). If a heterozygous individual (carrier) has both a dominant and a recessive allele, the dominant allele will be expressed, and the individual will not be affected by the grandchildless gene. When two carriers mate, there is a 25% chance that their offspring will inherit two recessive alleles and be affected by the gene.
02

Examining Drosophila reproductive biology

In Drosophila, as in many other organisms, male and female reproductive systems are different. Males produce sperm, while females produce eggs. During reproduction, the male's sperm fertilizes the female's eggs. The differences between male and female reproductive systems may contribute to the observed effect of the grandchildless gene only affecting the offspring of homozygous females.
03

Postulating why the grandchildless gene affects females but not males

One possible explanation for the grandchildless gene affecting the offspring of homozygous females and not homozygous males could be related to the gene's effect on the egg production or development in homozygous females. Since females contribute not only their genetic material but also the cytoplasm and other organelles to their offspring, it is plausible that the expression of the grandchildless gene leads to abnormalities in the egg's cytoplasm, which in turn impacts the development of the offspring and leads to sterility. In contrast, males contribute only genetic material in the form of sperm, and if the grandchildless gene has no effect on sperm development or function, the offspring of homozygous males would not be affected.
04

Observing the generational effect

In conclusion, the offspring of homozygous females carrying the recessive grandchildless gene are sterile, whereas the offspring of homozygous males are not. This can be attributed to the different roles of male and female reproductive systems, where the gene could have a detrimental effect on the egg's development in homozygous females. On the other hand, the lack of effect in offspring of homozygous males suggests that the mutant gene does not impact sperm development or function.

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Most popular questions from this chapter

Mutations in mitochondrial DNA appear to be responsible for a number of neurological disorders, including myoclonic epilepsy and ragged-red fiber disease, Leber's hereditary optic neuropathy, and Kearns-Sayre syndrome. In each case, the disease phenotype is expressed when the ratio of mutant to wild-type mitochondria exceeds a threshold peculiar to each disease, but usually in the 60 to 95 percent range. (a) Given that these are debilitating conditions, why has no cure been developed? Can you suggest a general approach that might be used to treat, or perhaps even cure, these disorders? (b) Compared with the vast number of mitochondria in an embryo, the number of mitochondria in an ovum is relatively small. Might such an ooplasmic mitochondrial bottleneck present an opportunity for therapy or cure? Explain.

A male mouse from a true-breeding strain of hyperactive animals is crossed with a female mouse from a true-breeding strain of lethargic animals. (These are both hypothetical strains.) All the progeny are lethargic. In the \(\mathrm{F}_{2}\) generation, all offspring are lethargic. What is the best genetic explanation for these observations? Propose a cross to test your explanation.

In this chapter, we focused on extranuclear inheritance and how traits can be determined by genetic information contained in mitochondria and chloroplasts, and we discussed how expression of maternal genotypes can affect the phenotype of an organism. At the same time, we found many opportunities to consider the methods and reasoning by which much of this information was acquired. From the explanations given in the chapter, what answers would you propose to the following fundamental questions? (a) How was it established that particular phenotypes are inherited as a result of genetic information present in the chloroplast rather than in the nucleus? (b) How did the discovery of three categories of petite mutations in yeast lead researchers to postulate extranuclear inheritance of colony size? (c) What observations support the endosymbiotic theory? (d) What key observations in crosses between dextrally and sinistrally coiled snails support the explanation that this phenotype is the result of maternal- effect inheritance? (e) What findings demonstrate a maternal effect as the basis of a mode of inheritance?

(a) In humans the mitochondrial genome encodes a low number of proteins, rRNAs, and tRNAs but imports approximately 1100 proteins encoded by the nuclear genome. Yet, with such a small proportion from the mitochondrial genome encoding proteins and RNAs, a disproportionately high number of genetic disorders due to mtDNA mutations have been identified (Bigger, B. et al. 1999 ). What inheritance pattern would you expect in a three-generation pedigree in which the grandfather expresses the initial mtDNA defect? What inheritance pattern would you expect in a three-generation pedigree in which the grandmother expresses the initial mtDNA defect? (b) Considering the description in part (a) above, how would your pedigrees change if you knew that the mutation that caused the mitochondrial defect was recessive and located in the nuclear genome, was successfully transported into mitochondria, and negated a physiologically important mitochondrial function?

Why is the rate of mutation in mitochondrial DNA higher than that in nuclear DNA but the incidence of genetic diseases caused by mutations in mitochondrial DNA relatively low?

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