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Streptomycin resistance in Chlamydomonas may result from a mutation in either a chloroplast gene or a nuclear gene. What phenotypic results would occur in a cross between a member of an \(m t^{+}\) strain resistant in both genes and a member of a strain sensitive to the antibiotic? What results would occur in the reciprocal cross?

Short Answer

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Additionally, what are the results of the reciprocal cross? Answer: The offspring of the initial cross, where the maternal parent is from the strain with streptomycin resistance in both the chloroplast and nuclear genes, will be phenotypically resistant to streptomycin. On the other hand, the offspring of the reciprocal cross, where the sensitive strain is the maternal parent, will be phenotypically sensitive to streptomycin.

Step by step solution

01

Understand the inheritance pattern and phenotype of streptomycin resistance in Chlamydomonas

Chlamydomonas is a unicellular green algae. The resistance to streptomycin in Chlamydomonas can be due to a mutation in either the chloroplast gene or the nuclear gene. The inheritance pattern of chloroplast genes is maternal, which means that they are inherited only from the maternal parent. On the other hand, nuclear genes are inherited from both parents in a Mendelian fashion. \(m t^{+}\) strain has a mutation in both the chloroplast and nuclear genes that causes resistance to streptomycin.
02

Determine the phenotypic results of the initial cross

In the initial cross, we have a member of the \(m t^{+}\) strain (resistant in both chloroplast and nuclear genes) as the maternal parent and a member of the sensitive strain as the paternal parent. The offspring will inherit the resistant chloroplast gene from their maternal parent (because chloroplast inheritance is maternal) and will also inherit one nuclear gene from each parent. As a result, the offspring will be heterozygous for nuclear gene (Nucleus R/n) and will have resistance in the chloroplast gene (Chloroplast R). Therefore, these offspring will be phenotypically resistant to streptomycin.
03

Determine the phenotypic results of the reciprocal cross

In the reciprocal cross, we have a member of the sensitive strain as the maternal parent and a member of the \(m t^{+}\) strain (resistant in both chloroplast and nuclear genes) as the paternal parent. The offspring will inherit the sensitive chloroplast gene from their maternal parent. The sensitive strain phenotype dominates over the resistant phenotype, and the offspring will be heterozygous for nuclear gene inheritance (Nucleus R/n). However, due to the dominant phenotype of the sensitive chloroplast gene, overall, the offspring will be phenotypically sensitive to streptomycin. In conclusion, the offspring of the initial cross, where the maternal parent is from the \(m t^{+}\) strain, will be phenotypically resistant to streptomycin. On the other hand, the offspring of the reciprocal cross, where the sensitive strain is the maternal parent, will be phenotypically sensitive to streptomycin.

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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.

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?

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 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?

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