Answer:
A) The two genes are unlinked and are assorting independently, leading to a 1:1:1:1 ratio of phenotypes in the offspring.
Explanation:
The χ2 value means nothing on its own--it is used to find the probability that, assuming the hypothesis is true, the observed data set could have resulted from random fluctuations. A low probability suggests the observed data is not consistent with the hypothesis, and thus the hypothesis should be rejected. The hypothesis that you are testing are two genes are unlinked and are assorting independently, leading to a 1:1:1:1 ratio of phenotypes in the offspring.
I believe it would be the bottleneck effect. hope that helps =)
Answer:
(A) It prevents electron flow from the iron-sulfur centers in complex 1 to the ubiquinone. Due to reduction in electron transfer rate, there is a decrease in the production of ATP which is dangerous for some insects and fish over time.
(B) It also prevents electron flow from cytochrome b to cytochrome c1 at the complex III which leads to QH2 accumulation. If oxidized Q is not present, these is alteration of electron flow and the production of ATP is altered.
(C) Rotenone only prevent electron transfer into the chain at Complex 1 but it does not affect electron transfer at Complex II. Although there is slow ETC, it does not stop completely. However, Antimycin A prevents the oxidation of QH2, the final electron acceptor crom complex I and complex II. Thereby, stopping the production of both ETC and ATP. It can be concluded that antimycin A is a more potent poison.
Explanation:
Rotenone prevents electron flow from the iron-sulfur centers in complex 1 to the ubiquinone. Due to a reduction in electron transfer rate, there is a decrease in the production of ATP which is dangerous for some insects and fish over time. Antimycin A also prevents electron flow from cytochrome b to cytochrome c1 at the complex III which leads to QH2 accumulation. If oxidized Q is not present, there is an alteration of electron flow and the production of ATP is altered. Antimycin A is more potent than rotenone.
Answer:
Genetic mapping for unequivocal identification of the potentially causative mutation
Explanation:
Galactosemia is a genetic disorder caused by mutations in the Galactose-1-phosphate uridylyltransferase (GALT) gene, which encodes an enzyme involved in the metabolism of galactose. Gene mapping is a technique widely used in genetics to identify the position of one locus a chromosome by using molecular markers to estimate genetic distances. Genetic mapping provides useful evidence in order to identify when a disease that is transmitted from parent to offspring can be associated with one or more genes and then determine which gene/s is/are responsible for this condition.
