You have isolated a temperature-sensitive mutant that, at the restrictive temper

Question

You have isolated a temperature-sensitive mutant that, at the restrictive temperature, has no ability to translocated proteins into mitochondria. So far you have eliminated any of the proteins forming the various transporters (TOM complex, SAM complex, TIM22 complex, TIM23 complex and OXA complex) and the porin proteins as candidates for the mutation. In other words, all the transporter proteins are wild type. What is your hypothesis for a protein that may be responsible for this mutant phenotype.

Explanation / Answer

Translocation of proteins into the mitochondria is an important physiological process which determines the homeostatic functionality of mitochondria. The translocation is dependent upon the mitochondrial membrane bound receptors on the surface of the mitochondria and the translocators in the outer and inner membrane of the mitochondria that mediate the import and intra-mitochondrial sorting of these proteins. When the transporters like (TOM complex, SAM complex, TIM22 complex, TIM23 complex and OXA complex) and the porin proteins are eliminated from the mutation candidate list, then the most probable candidate would be in the receptors that could not receive the protein after th temperature-sensitive mutation.

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