supose that there is a mutation in a single-celled organism where the kreb cycle is does not happen. What would be the consequences for that organism? How would their metabolism be similar to ours? How would it be different?

Researchers isolated a yeast phosphofructokinase (PFK) mutant in which a serine at the fructose-2,6-bisphosphate binding site was replaced with an aspartate residue. The amino acid substitution completely abolished the binding of fructose-2,6-bisphosphate to PFK. There was a dramatic decline in glucose consumption and ethanol production in the mutant compared to control yeast. Why can't the mutant PFK bind with fructose-2,6-bisphosphate?

You are studying a bacterial metabolic pathway that results in the synthesis of a product, vitalin, that is essential for survival. In the figure below, each number represents an intermediate product, and each letter represents the enzyme (protein) that catalyzes that step. 3 >5'> Vitalin a Compound -"> 1 – Z. 4 > Vitalin You find that bacteria with mutations in either c or f can survive, but a bacterial cell that has mutations in both c and f cannot survive. For every mutation, assume that the bacteria have other functional proteins in the pathway. Which of the following mutants can grow on media containing only intermediate 3? Select all that apply Mutant f Mutant b Mutant d Mutant c

You are studying a bacterial metabolic pathway that results in the synthesis of a product, vitalin, that is essential for survival. In the figure below, each number represents an intermediate product, and each letter represents the enzyme (protein) that catalyzes that step. d 3 e 5 Vitalin Compound 4 > Vitalin You find that bacteria with mutations in either c orf can survive, but a bacterial cell that has mutations in both c and f cannot survive. Which of the following statements explain your observations? Select all that apply. If both genes, c and f, are mutated, then vitalin cannot be synthesized O If gene c is mutated, then vitalin cannot be synthesized The pathway to synthesis of vitalin is branched, and either one can result in vitalin production gene c is mutated, then bacteria can survive by synthesizing vitalin using enzymes f and g If

Of all the genes in the human genome, the ones withthe most characterized Alu insertions are those thatcause hemophilia, including several insertions in thefactor VIII and factor IX genes. Based on this fact, yourcolleague hypothesizes that the Alu element prefers toinsert into these genes. Do you agree? What other reason can you provide that also explains these data?

Suppose you want to figure out what genes are involved in the production of proline (Pro) in a certain bacteria.   (1) How would you go about designing a mutant screen to do so? (2) Suppose your screen identified 5 mutants that barely grew without being given Pro in the medium. How would you go about determining the number of different genes these mutants represent?

In the Q Cycle of Complex III, the two electrons from QH2 are split up and go to different places. Why must the electrons be split up?

In the experiment of Figure shown , a met− bio− thr+ leu+ thi+ cellcould become met+ bio+ thr+ leu+ thi+ by a (rare) double mutationthat converts the met− bio− genes into met+ bio+. Likewise, a met+bio+ thr− leu− thi− cell could become met+ bio+ thr+ leu+ thi+ bythree mutations that convert the thr− leu− thi− genes into thr+ leu+thi+. From the results of Figure shown, how do you know that the occurrenceof 10 met+ bio+ thr+ leu+ thi+ colonies is not due to thesetypes of rare double or triple mutations?

Can you please answer 18, and 19

Galactosemia is a metabolic disorder characterized by the inability to metabolize the sugar galactose. People with galactosemia suffer from liver, kidney, and brain damage among other symptoms. A gene mutation underlying galactosemia was identified by sequencing the genome of a person with galactosemia. What additional evidence would support the hypothesis that the mutation in the candidate gene causes the disease?