Unit 9: Regulation of Gene Expression
How bacteria switch whole gene sets on and off in response to their environment, and the layered controls eukaryotic cells add on top.
7 topics · 25 questions
Each topic is a path, not a menu: work down it in order and every question builds on the one above. Click any of them to watch the answer draw itself.
The Lac Operon and Inducible Regulation
- How it worksHow does the lac repressor block transcription of the lac operon until lactose is present?
- Worked exampleTrace the lac operon's transcription state across all four combinations of glucose present or absent and lactose present or absent.
- Common mistakeWhy doesn't the lac operon turn on the instant any lactose at all appears, regardless of glucose levels?
- Going furtherWhat happens to lac operon transcription in a bacterium whose repressor gene is mutated and can never bind the operator?
Your turn1 of 2
Both glucose and lactose are present in an E. coli cell's environment. Lactose alone would normally induce the lac operon, but the operon stays only weakly transcribed as long as glucose is around. Why doesn't the lac operon turn on fully the instant any lactose appears, regardless of glucose levels?The Trp Operon and Repressible Regulation
- How it worksHow does tryptophan acting as a corepressor activate the trp repressor to block transcription?
- How it worksHow does attenuation fine-tune trp operon transcription based on how fast a ribosome translates the leader peptide?
- Ties togetherHow does the trp operon's repressible logic contrast with the lac operon's inducible logic while using the same basic on-off design?
- Worked exampleFind whether the trp operon is transcribed given tryptophan levels are low and no repressor is bound to the operator.
Your turn1 of 2
In attenuation, when tryptophan is abundant, a ribosome translates the trp operon's short leader peptide quickly, without stalling, which promotes early termination of transcription. When tryptophan is scarce, the ribosome stalls at trp codons in the leader sequence. How does this ribosome speed fine-tune transcription of the downstream trp genes?Eukaryotic Transcription Factors, Promoters, and Enhancers
- How it worksHow does an enhancer loop DNA around to bring transcription factors into contact with a distant promoter?
- Common mistakeWhy doesn't an enhancer need to sit right next to the gene it regulates the way a bacterial operator does?
- Going furtherWhat happens to a gene's expression pattern when a mutation destroys the binding site for one of its transcription factors?
Your turn1 of 2
A bacterial operator sequence must sit immediately next to the gene it controls, but a eukaryotic enhancer can sit tens of thousands of bases away and still control a gene's transcription. Why doesn't a eukaryotic enhancer need to be right next to its target gene?Chromatin Structure and Gene Accessibility
- How it worksHow does DNA wrapping tightly around histones in heterochromatin physically block transcription machinery from reaching a gene?
- Worked exampleTrace how histone acetylation loosens chromatin at a gene's promoter and switches transcription on.
- Common mistakeWhy doesn't every cell in the body need to unwind all of its DNA in order to survive?
- Going furtherWhat happens to a gene's transcription when a histone deacetylase removes acetyl groups from its promoter region?
Your turn1 of 2
Every cell in the body carries the same complete genome, yet each cell type only actively transcribes a small fraction of it. Why doesn't every cell need to unwind ALL of its DNA in order to survive?Epigenetics: DNA Methylation and Histone Modification
- How it worksHow does adding a methyl group to cytosine bases in a promoter silence a gene without changing its DNA sequence?
- Going furtherWhat happens to a cell's epigenetic marks when it divides, and how do they get copied onto the daughter cell's DNA?
- Common mistakeWhy isn't an epigenetic change the same thing as a mutation in the underlying DNA sequence?
Your turn1 of 2
An epigenetic change, like adding methyl groups to a gene's promoter, can silence that gene just as effectively as a mutation would. Why isn't an epigenetic change actually the same thing as a mutation in the underlying DNA sequence?Genomic Imprinting
- How it worksHow does methylation established during egg and sperm formation silence one parent's copy of an imprinted gene?
- Worked exampleTrace the inheritance pattern of Prader-Willi syndrome when the paternal copy of the imprinted region is deleted.
- Common mistakeWhy doesn't genomic imprinting follow the same dominant-recessive logic as an ordinary autosomal gene?
- Worked exampleFind which parent's copy of a gene ends up expressed when only the maternal allele carries the silencing imprint.
Your turn1 of 2
For an ordinary autosomal gene, dominant-recessive logic determines phenotype from genotype regardless of which parent contributed which allele. For an imprinted gene, however, whether an allele is expressed can depend entirely on WHICH PARENT it came from. How is this different from both maternal effect inheritance and mitochondrial inheritance, which also involve a parent-of-origin pattern?Post-Transcriptional and Post-Translational Regulation
- How it worksHow does a microRNA binding to an mRNA's untranslated region block translation or trigger its degradation?
- How it worksHow does adding a ubiquitin tag mark a finished protein for destruction by the proteasome?
- Ties togetherHow do post-transcriptional and post-translational controls add a second layer of regulation on top of an operon's on-off switch?
Your turn1 of 2
A microRNA in the cytoplasm binds to a complementary sequence in the 3' untranslated region of a target mRNA. This binding never touches the gene itself or its promoter. How does it still reduce how much protein that gene's mRNA produces?