7–8 The nucleus of a eukaryotic cell is much larger than a bacterium, and it contains much more DNA. As a consequence, a transcription regulator in a eukaryotic cell must be able to select its specific binding site from among many more unrelated sequences than does a transcription regulator in a bacterium. Does this present any special problems for eukaryotic gene regulation?
Consider the following situation. Assume that the eukaryotic nucleus and the bacterial cell each have a single copy of the same DNA binding site. In addition, assume that the nucleus is 500 times the volume of the bacterium, and has 500 times as much DNA. If the concentration of the transcription regulator that binds the site were the same in the nucleus and in the bacterium, would the regulator occupy its binding site equally as well in the eukaryotic nucleus as it does in the bacterium? Explain your answer.
7–9 Some transcription regulators bind to DNA and cause the double helix to bend at a sharp angle. Such “bending proteins” can affect the initiation of transcription without directly contacting any other protein. Can you devise a plausible explanation for how such proteins might work to modulate transcription? Draw a diagram that illustrates your explanation.
7–10 How is it that protein–protein interactions that are too weak to cause proteins to assemble in solution can nevertheless allow the same proteins to assemble into complexes on DNA?
7–11 Imagine the two situations shown in Figure Q7–2. In cell 1, a transient signal induces the synthesis of protein A, which is a transcription activator that turns on many genes including its own. In cell 2, a transient signal induces the synthesis of protein R, which is a transcription repressor that turns off many genes including its own. In which, if either, of these situations will the descendants of the original cell “remember” that the progenitor cell had experienced the transient signal? Explain your reasoning.
transcription turns on transcription activator protein activator of activator mRNA turns on its own transcription
Figure Q7–2 Gene regulatory circuits and cell memory (problem 7–11).
(A) induction of synthesis of transcription activator A by a transient signal. (B) induction of synthesis of transcription repressor r by a transient signal.
7–12 Examine the two pedigrees shown in Figure Q7–3. One results from deletion of a maternally imprinted autosomal gene. The other pedigree results from deletion of a paternally imprinted autosomal gene. In both pedigrees, affected individuals (red symbols) are heterozygous for the deletion. These individuals are affected because one copy of the chromosome carries an imprinted, inactive gene, while the other carries a deletion of the gene. Dotted yellow symbols indicate individuals that carry the deleted locus, but do not display the mutant phenotype. Which pedigree is based on paternal imprinting and which on maternal imprinting? Explain your answer.
Figure Q7–3 pedigrees reflecting maternal and paternal imprinting (problem 7–12). in one pedigree, the gene is paternally imprinted; in the other, it is maternally imprinted. in generations 3 and 4, only one of the two parents in the indicated matings is shown; the other parent is a normal individual from outside this pedigree. Affected individuals are represented by red circles for females and red squares for males. Dotted yellow symbols indicate individuals that carry the deletion but do not display the phenotype.
7–13 If you insert a β-galactosidase gene lacking its own transcription control region into a cluster of piRNA genes in Drosophila, you find that β-galactosidase expression from a normal copy elsewhere in the genome is strongly inhibited in the fly’s germ cells. If the inactive β-galactosidase gene is inserted outside the piRNA gene cluster, the normal gene is properly expressed. What do you suppose is the basis for this observation? How would you test your hypothesis?
Brown tA (2007) Genomes 3. new York: Garland Science.