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09:16 09:16The UG4 gene is expressed in stem tissue and leaf tissue of the plant Arabidopsis thaliana. To study mechanisms regulating UG4 expression, six small deletions of DNA sequence upstream of the gene-coding sequence are made. The locations of deletions and their effect on UG4 expression are shown here. Why does deletion D raise UG4 expression in leaf tissue but not in stem tissue?
The UG4 gene is expressed in stem tissue and leaf tissue of the plant Arabidopsis thaliana. To study mechanisms regulating UG4 expression, six small deletions of DNA sequence upstream of the gene-coding sequence are made. The locations of deletions and their effect on UG4 expression are shown here. Why does deletion E lower expression of UG4 in leaf tissue but not in stem tissue?
Diagram and explain how the inducibility of a gene—for instance in response to an environmental cue—could be mediated by an activator. Then show how it could be mediated by a repressor.
A muscle enzyme called ME1 is produced by transcription and translation of the ME1 gene in several muscles during mouse development, including heart muscle, in a highly regulated manner. Production of ME1 appears to be turned on and turned off at different times during development. To test the possible role of enhancers and silencers in ME1 transcription, a biologist creates a recombinant genetic system that fuses the ME1 promoter, along with DNA that is upstream of the promoter, to the bacterial lacZ (β-galactosidase) gene. The lacZ gene is chosen for the ease and simplicity of assaying production of the encoded enzyme. The diagram shows bars that indicate the extent of six deletions the biologist makes to the ME1 promoter and upstream sequences. The blue deletion labeled D is within the promoter whereas the gray bars span potential enhancer/silencer modules. The table displays the percentage of β-galactosidase activity in each deletion mutant in comparison with the recombinant gene system without any deletions.
Why does deletion D effectively eliminate transcription of lacZ?
A muscle enzyme called ME1 is produced by transcription and translation of the ME1 gene in several muscles during mouse development, including heart muscle, in a highly regulated manner. Production of ME1 appears to be turned on and turned off at different times during development. To test the possible role of enhancers and silencers in ME1 transcription, a biologist creates a recombinant genetic system that fuses the ME1 promoter, along with DNA that is upstream of the promoter, to the bacterial lacZ (β-galactosidase) gene. The lacZ gene is chosen for the ease and simplicity of assaying production of the encoded enzyme. The diagram shows bars that indicate the extent of six deletions the biologist makes to the ME1 promoter and upstream sequences. The blue deletion labeled D is within the promoter whereas the gray bars span potential enhancer/silencer modules. The table displays the percentage of β-galactosidase activity in each deletion mutant in comparison with the recombinant gene system without any deletions.
Given the information available from deletion analysis, can you give a molecular explanation for the observation that ME1 expression appears to turn on and turn off at various times during normal mouse development?
Using the components in the accompanying diagram, design regulatory modules (i.e., enhancer/silencer modules) required for 'your' gene to be expressed only in differentiating (early) and differentiated (late) liver cells. Answer the three questions presented below by describing the roles that activators, enhancers, repressors, silencers, pioneer factors, insulators, chromatin remodeling complexes, and chromatin readers, writers, and erasers will play in the regulation of expression of your gene, that is, what factors will bind and be active in each case? Specify which transcription factors need to be pioneer factors. How will the gene be activated in the proper cell type?
