Becker's World of the Cell 9th Edition by Lewis Kleinsmith, Jeff Hardin, Gregory Paul Bertoni

Exercise 3

Regulation of Bellicose Catabolism. The enzymes bellicose kinase and bellicose phosphate dehydrogenase are coordinately regulated in the bacterium Hokus focus. The genes encoding these proteins, belA and belB, are contiguous segments on the genetic map of the organism. In her pioneering work on this system, Professor Jean X. Pression established that the bacterium can grow with the monosaccharide bellicose as its only carbon and energy source, that the two enzymes involved in bellicose catabolism are synthesized by the bacterium only when bellicose is present in the medium, and that enzyme production is turned off in the presence of glucose. She identified a number of mutations that reduce or eliminate enzyme production and showed these could be grouped into two classes. Class I mutants are in ds-acting elements, whereas those in class II all map at a distance from the genes coding for the enzymes and are irans-acting. Thus far, the only constitutive mutations Pression has found are deletions that connect belA and belB to new DNA at the upstream side of belA. The following is a list of conclusions she would like to draw from her observations. Indicate in each case whether the conclusion is consistent with the data (C), inconsistent with the data (I), or irrelevant to the data (X).
(a)Bellicose can be metabolized by H. focus cells to yield ATP.
(b)Enzyme production by genes belA and belB is under positive control.
(c)Phosphorylation of bellicose makes the sugar less permeable to transport across the plasma membrane.
(d)The operator for the bellicose operon is located upstream from the promoter.
(e)Some of the mutations in class I may be in the promoter.
(f)Some of the mutations in class II may be in the operator.
(g)Class II mutations may include mutations in the gene that encodes CAP.
(h)The constitutive deletion mutations connect genes belA and belB to a new promoter.
(i)Expression of the bellicose operon is subject to regulation by attenuation.