Ch. 9 - Extranuclear Inheritance

Klug - Concepts of Genetics 12th Edition

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Klug 12th Edition

Ch. 9 - Extranuclear Inheritance

Problem 16

Chapter 9, Problem 16

The maternal-effect mutation bicoid (bcd) 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 (bcd⁺/bcd⁻) and a male homozygous for the mutation (bcd⁻/bcd⁻).
Predict the outcome (normal vs. failed embryogenesis) in the F₁ and F₂ generations of the cross described.

Verified step by step guidance

Step 1: Understand the concept of maternal-effect genes. Maternal-effect genes are genes whose products are provided by the mother and are required for early embryonic development. The phenotype of the offspring is determined by the genotype of the mother, not the offspring itself.

Step 2: Analyze the parental genotypes. The female parent is heterozygous (bcd⁺/bcd⁻), meaning she has one functional allele (bcd⁺) and one mutant allele (bcd⁻). The male parent is homozygous for the mutant allele (bcd⁻/bcd⁻), meaning he contributes no functional bicoid protein.

Step 3: Predict the F₁ generation outcome. Since the maternal genotype determines embryogenesis, the heterozygous female (bcd⁺/bcd⁻) will provide sufficient bicoid protein for embryogenesis in her offspring, regardless of their genotype. Therefore, all F₁ embryos will develop normally.

Step 4: Predict the F₂ generation outcome. To determine the F₂ generation, consider the genotypes of the F₁ individuals. If an F₁ female is heterozygous (bcd⁺/bcd⁻) and mates with an F₁ male (bcd⁻/bcd⁻), the maternal genotype of the F₂ offspring will determine their embryogenesis. If the F₂ female is homozygous mutant (bcd⁻/bcd⁻), she will not provide functional bicoid protein, leading to failed embryogenesis in her offspring.

Step 5: Summarize the outcomes. In the F₁ generation, all embryos develop normally due to the maternal heterozygous genotype. In the F₂ generation, embryogenesis will fail for offspring of homozygous mutant (bcd⁻/bcd⁻) females, while offspring of heterozygous (bcd⁺/bcd⁻) females will develop normally.

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Key Concepts

Here are the essential concepts you must grasp in order to answer the question correctly.

Maternal-effect genes

Maternal-effect genes are genes expressed in the mother that influence the development of the offspring, regardless of the offspring's own genotype. The bicoid gene is a classic example, where the presence of the bicoid protein in the egg is crucial for proper embryonic development. If the mother is homozygous for a recessive mutation, the offspring will inherit the effects of that mutation, leading to developmental failures.

Recessive alleles

Recessive alleles are variants of a gene that do not manifest their traits in the presence of a dominant allele. In the case of the bicoid mutation, the bcd⁻ allele is recessive, meaning that an individual must inherit two copies of this allele (bcd⁻/bcd⁻) to exhibit the associated phenotype. Understanding how recessive alleles function is essential for predicting the outcomes of genetic crosses.

Punnett square and genetic crosses

A Punnett square is a tool used to predict the genotypic and phenotypic outcomes of genetic crosses. By organizing the alleles of the parents, one can visualize the possible combinations in the offspring. In this scenario, analyzing the cross between a heterozygous female and a homozygous recessive male will help determine the likelihood of normal versus failed embryogenesis in the F₁ and F₂ generations.

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Textbook Question

Earlier, we described CC, the cat created by nuclear transfer cloning, whereby a diploid nucleus from one cell is injected into an enucleated egg cell to create an embryo. Cattle, sheep, rats, dogs, and several other species have been cloned using nuclei from somatic cells. Embryos and adults produced by this approach often show a number of different mitochondrial defects. Explain possible reasons for the prevalence of mitochondrial defects in embryos created by nuclear transfer cloning.

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Textbook Question

Mitochondrial replacement therapy (MRT) offers a potential solution for women with mtDNA-based diseases to have healthy children. Based on what you know about the importance of nuclear gene products to mitochondrial functions, will MRT ensure that children will not inherit or develop a mtDNA-based diseases?

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Textbook Question

The specification of the anterior–posterior axis in Drosophila embryos is initially controlled by various gene products that are synthesized and stored in the mature egg following oogenesis. Mutations in these genes result in abnormalities of the axis during embryogenesis. These mutations illustrate maternal effect. How do such mutations vary from those produced by organelle heredity? Devise a set of parallel crosses and expected outcomes involving mutant genes that contrast maternal effect and organelle heredity.

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Textbook Question

The maternal-effect mutation bicoid (bcd) 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 (bcd⁺/bcd⁻) and a male homozygous for the mutation (bcd⁻/bcd⁻).

How is it possible for a male homozygous for the mutation to exist?

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Textbook Question

(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?

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Textbook Question

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.

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?

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