A. Since it takes 40 min. to replicate the E. coli chromosome,how can the cell have a cell cycle of 35 minutes?
B.What would happen to a bacterial chromosome during celldivision if it were not connected to the membrane?
C. How do eukaryotes divide their pairs of chromosomes into twoseparate cells?
D. How could you isolate a loss of function mutation is anessential gene when mutating the gene can kill the cell?
E. How is it possible that a single gene like ftsZ can havemutations that have different phenotypes?
F. What would minC mutant bacterial look like?
G.Why is recombination after replication only a problem fro abacterium that has a circular chromosome and not a linearchromosome?
H.Why do bacterial have to attach their chromosomes to themembrane for effective separation, whereas eukarotes do not?
I.Why is the classical signal transduction pathway so complex,why not simply have the growth factor receptor activate thetranscription factor?
J.What is the phenotype of a cell that is heterozygous for a RASoncogenic mutation?
K. How does p53 communicate with Rb?
L. What is the phenotype of a cell that is heterozygous for aloss of function p53 mutant?
M. Rb is only acted upon by Cyclin/CDK, how can it integrate DNAdamage signal from p53?
A. Since it takes 40 min. to replicate the E. coli chromosome,how can the cell have a cell cycle of 35 minutes?
B.What would happen to a bacterial chromosome during celldivision if it were not connected to the membrane?
C. How do eukaryotes divide their pairs of chromosomes into twoseparate cells?
D. How could you isolate a loss of function mutation is anessential gene when mutating the gene can kill the cell?
E. How is it possible that a single gene like ftsZ can havemutations that have different phenotypes?
F. What would minC mutant bacterial look like?
G.Why is recombination after replication only a problem fro abacterium that has a circular chromosome and not a linearchromosome?
H.Why do bacterial have to attach their chromosomes to themembrane for effective separation, whereas eukarotes do not?
I.Why is the classical signal transduction pathway so complex,why not simply have the growth factor receptor activate thetranscription factor?
J.What is the phenotype of a cell that is heterozygous for a RASoncogenic mutation?
K. How does p53 communicate with Rb?
L. What is the phenotype of a cell that is heterozygous for aloss of function p53 mutant?
M. Rb is only acted upon by Cyclin/CDK, how can it integrate DNAdamage signal from p53?
