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The maternal-effect mutation bicoid ( \(b c d\) ) is recessive. In the absence of the bicoid protein product, embryogenesis is not completed. Consider a cross between a female heterozygous for the bicoid alleles \(\left(b c d^{+} / b c d^{-}\right)\) and a male homozygous for the mutation \(\left(b c d^{-} / b c d^{-}\right)\) (a) How is it possible for a male homozygous for the mutation to exist?. (b) Predict the outcome (normal vs. failed embryogenesis) in the \(\mathrm{F}_{1}\) and \(\mathrm{F}_{2}\) generations of the cross described.

Short Answer

Expert verified
Is it possible for a male to have two recessive alleles for bicoid? Answer: When a heterozygous female (bcd+/bcd-) mates with a homozygous male (bcd-/bcd-) for the bicoid gene, the resulting F1 generation offspring will all be heterozygous (bcd+/bcd-), but they will develop normally due to sufficient bicoid proteins received from their mother during embryogenesis. It is possible for a male to have two recessive alleles for bicoid if the mother provides enough normal bicoid proteins during oogenesis, allowing the mutant father to survive. The F2 generation outcomes depend on maternal genotypes, with a 75% chance of normal embryogenesis and a 25% chance of failed embryogenesis for offspring inheriting at least one normal allele from their mother.

Step by step solution

01

Identify the genotypes

The female in the cross is heterozygous, meaning she has one normal allele (bcd+) and one mutated allele (bcd-) for bicoid. The genotype of the female is thus represented as bcd+/bcd-. The male is homozygous for the mutation, meaning he has two mutated alleles (bcd-) for bicoid. The genotype of the male is represented as bcd-/bcd-.
02

Discuss the possibility of a male homozygous for the mutation

The bicoid mutation affects embryogenesis; however, a male homozygous for the mutation can exist if the mother provides sufficient normal bicoid proteins during oogenesis (the female process of producing eggs). This maternal effect allows mutant fathers to survive, but they will always pass a mutated allele to their offspring.
03

Predict the F1 generation outcomes

In the F1 generation, the heterozygous female will provide normal bicoid proteins during oogenesis. Thus, she will pass one mutated allele (bcd-) and sufficient normal bicoid proteins required for the embryogenesis process. The homozygous male will pass one mutated allele (bcd-). The resulting offspring will have a genotype of bcd+/bcd-, making them all heterozygous. However, due to the sufficient bicoid proteins received from their mother during embryogenesis, they will develop normally.
04

Predict the F2 generation outcomes

In the F2 generation, the offspring are all heterozygous (bcd+/bcd-). When breeding occurs within the F2 generation, there are three possible genotype combinations: 1. bcd+/bcd+ (normal mother, able to provide bicoid proteins) 2. bcd+/bcd- (normal mother, able to provide bicoid proteins) 3. bcd-/bcd- (potentially normal, depending on maternally inherited proteins) If the mother is bcd+/bcd+ or bcd+/bcd-, she will pass on the required normal bicoid proteins for embryogenesis. The offspring in the F2 generation will have a 75% chance of normal embryogenesis and a 25% chance of failed embryogenesis, regardless of their own inherited genotype. The chances of a failed embryogenesis increase only if the mother has the genotype bcd-/bcd-, as she cannot provide the necessary bicoid proteins. In this case, all the offspring of such a female will have failed embryogenesis.

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Most popular questions from this chapter

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.

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.

Compare the molecular organization in mitochondrial DNA with that in chloroplast DNA.

Tools are now available to sequence mtDNAs from an individual's genome sequence data to accurately measure heteroplasmy and to easily recognize the most functionally important mitochondrial variants. What is the significance of these tools for the diagnosis of human mtDNA diseases? If your sibling is diagnosed with a mitochondrial degenerative neurological disorder, would you want your mtDNA to be sequenced for mutations and heteroplasmy?

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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