Gene Expression Regulation Tournament
Two onboarding diagrams orient you in the transcription control network. Then eight MCAT-DoK quiz rounds: allolactose and lac induction, catabolite repression when glucose and lactose are both around, the steroid nuclear-receptor cascade, cis elements from the TATA box to distant enhancers, polycistronic operon architecture, the epigenetic marks behind imprinting and the Barr body, miRNA silencing, and trp attenuation.
Where the Epigenetic regulation of gene expression fits in Gene expression (transcription)
Reactome's transcription map covers all three eukaryotic RNA polymerases - Pol I for rRNA, Pol II for mRNA, Pol III for tRNA - along with the regulatory layers stacked above them. The highlighted epigenetics panel is the chromatin-level control that decides which genes a polymerase can physically reach in the first place, long before any promoter is read. Click the highlighted Epigenetic regulation panel to enter the tournament.
Click the highlighted Epigenetic regulation of gene expression box to continue.
What this tournament tests
Each task maps to a distinct MCAT cognitive demand. The first two orient you in the broader topology; the next eight test the high-yield mechanism, regulation, sequence and quantitative reasoning that consistently appear on test day.
The Bigger Picture
Anchor epigenetic control inside the full transcription pathway on the live Reactome map.
Whole-Pathway Overview
Pan and zoom the curated WikiPathways histone-modification figure before you start answering.
Fill in the Blank
Recall allolactose as the inducer that pulls the lac repressor off the operator.
Disruptor
Explain why glucose plus lactose still yields almost no lac expression - low cAMP means no CAP.
Sequence Ordering
Trace a steroid hormone from membrane diffusion -> intracellular receptor -> response element -> new protein.
Match the Pairs
Pair TATA box, enhancer, silencer, operator, HAT, HDAC, DNA methyltransferase, and miRNA with their exact jobs.
Numeric Input
Recall how many structural genes ride on the single polycistronic lac transcript.
Select All That Apply
Identify TRUE statements on histone acetylation, CpG methylation, imprinting, the Barr body, and alternative splicing.
Odd One Out
Separate post-transcriptional miRNA silencing from three transcription-initiation mechanisms.
Trp Operon Disruptor
Recognize tryptophan as a corepressor and explain attenuation in a repressible operon.
Public leaderboard
Your score posts to a global, persistent leaderboard scored by points first, time as tiebreaker.
Gene regulation in 60 seconds
Bacteria bundle related genes into operons read as one polycistronic mRNA. The lac operon is inducible and runs on two layers: negative control, where allolactose removes the repressor from the operator, and positive control, where low glucose raises cAMP so CAP can bind and recruit RNA polymerase to a weak promoter. Both conditions must be met - lactose present AND glucose absent - which is why glucose plus lactose gives almost nothing. The trp operon is the mirror image: repressible, with tryptophan acting as a corepressor and attenuation adding a second, finer dial.
Eukaryotes have no operons. Each gene is regulated individually through cis elements: a core promoter with the TATA box about 25 bp upstream, plus enhancers and silencers that can act thousands of base pairs away, in either orientation, and even from inside an intron, because the DNA loops back to the promoter. The transcription factors that read those elements are modular, with a separable DNA-binding domain and activation domain - which is exactly what lets a two-hybrid or domain-swap experiment work.
Above all of that sits chromatin. HATs acetylate lysines, neutralize the positive charge histones use to grip DNA, and open the region into transcriptionally active euchromatin; HDACs strip those acetyl groups and recondense it into heterochromatin. DNA methylation of promoter CpG islands silences genes and is copied to the daughter strand after replication, making it heritable. That heritability is the basis of genomic imprinting (Prader-Willi vs Angelman at 15q11-q13) and of X-inactivation, which condenses one X into the Barr body.
Control does not stop at transcription. Alternative splicing lets one gene yield several protein isoforms, and microRNAs loaded into RISC pair with a target mRNA - usually in the 3' UTR - to block translation or trigger degradation. Steroid hormones plug straight into this system: being lipid soluble they cross the membrane, bind an intracellular receptor that is itself a transcription factor, and the complex binds a hormone response element directly. That is why steroids act slowly (hours, new protein required) but persistently, while peptide hormones on surface receptors act in seconds -> second messenger -> existing enzymes.
FAQ
What is the difference between an inducible and a repressible operon?
An inducible operon is normally OFF and is switched ON by its substrate - the lac operon, where allolactose inactivates the repressor. A repressible operon is normally ON and is switched OFF by its end product - the trp operon, where tryptophan acts as a corepressor that activates the repressor. Rule of thumb: catabolic pathways are inducible (make the enzyme when the food shows up), anabolic pathways are repressible (stop making the enzyme when you already have the product).
Why does glucose block lac expression even when lactose is present?
This is catabolite repression, and it works through positive control, not the repressor. High glucose keeps cAMP low, so CAP cannot bind upstream of the lac promoter. The lac promoter is weak on its own, so RNA polymerase binds poorly and transcription stays near baseline even though allolactose has already removed the repressor. When glucose runs out, cAMP rises, CAP binds and bends the DNA, and lac expression surges - the second phase of diauxic growth.
How can enhancers work from thousands of base pairs away?
The DNA loops. An activator protein binds the enhancer, and looping brings that activator into physical contact with the mediator complex and the general transcription machinery at the promoter. Because the contact is made in three dimensions rather than by scanning along the strand, enhancers work at long distances, in either orientation, and from upstream, downstream, or inside an intron - all facts the MCAT likes to test as a single trap answer.
Are epigenetic changes permanent?
No. Histone acetylation and DNA methylation change which genes are read without altering the underlying base sequence, and they can be reversed - HDACs remove acetyl groups, demethylases remove methyl marks. They are heritable through cell division because methylation patterns are copied onto the daughter strand after replication, which is what makes imprinting and X-inactivation stable within a cell lineage. Reversibility is also why HDAC inhibitors and DNA methyltransferase inhibitors exist as real drug classes.
Do I need an account to play?
No. The tournament is fully public. You get a randomized handle and your score posts to the public leaderboard at the bottom of this page.
Keep going
The machinery being regulated - RNA polymerase II, the general transcription factors, and pre-mRNA processing.
The next control point once an mRNA exists - initiation factors, the ribosome, and where miRNAs block the message.
Overview diagram: Reactome Pathway R-HSA-74160, licensed CC BY 4.0.