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?
How did the discovery of three categories of petite mutations in yeast lead researchers to postulate extranuclear inheritance of colony size?
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?
What observations support the endosymbiotic theory?
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Verified Solution
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Key Concepts
Endosymbiotic Theory
Extranuclear Inheritance
Phenotype and Maternal Genotypes
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 mt⁺ strain resistant in both genes and a member of a strain sensitive to the antibiotic? What results would occur in the reciprocal cross?
What is the endosymbiotic theory, and why is this theory relevant to the study of extranuclear DNA in eukaryotic organelles?
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?