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 D raise UG4 expression in leaf tissue but not in stem tissue?

Competing endogenous RNAs act as molecular 'sponges.' What does this mean, and what do they compete with?

While circular RNAs were first described long ago, they have only recently been investigated for function. What are their known and suspected functions in the cell?

How are mRNAs stored within the cell in a translationally inactive state, and how can their translation be stimulated?

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.

How and why are eukaryotic mRNAs transported and localized to discrete regions of the cell?

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?