Operons and Prokaryotic Control and Eukaryotic Gene Control and Cancer | Six Minutes: MCAT, Part 9
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Operons and Prokaryotic Control and Eukaryotic Gene Control and Cancer | Six Minutes: MCAT, Part 9
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Six Minutes: MCAT, Part 9: Operons and Prokaryotic Control and Eukaryotic Gene Control and Cancer: B/B 1B: the Jacob-Monod model, repression, and positive control; then Eukaryotic Gene Control and Cancer
Bacteria group related genes into operons controlled by a promoter and an operator. This episode explains the Jacob-Monod model, gene repression, and positive control, then works through a two-signal regulation problem. Then: Eukaryotic genes are controlled in layers: chromatin packing, DNA methylation, transcription factors, alternative splicing, amplification, and noncoding RNAs. Cancer arises when control breaks, through overactive oncogenes, lost tumor suppressors, and telomerase that keeps telomeres long.
Chapters
0:00 Introduction
0:23 The operon idea
0:45 Negative control: repression
1:24 Positive control
1:41 Worked example
2:41 The trap
3:02 Recap
3:20 Eukaryotic Gene Control and Cancer
3:33 Layers of control
4:37 Splicing and amplification
5:10 When control breaks
5:50 Worked example
6:41 The trap
6:57 Recap
7:19 Thanks for watching
Practice problems
1. In a made-up operon, a repressor binds the operator unless sugar X is present. If sugar X is added to cells, what happens to transcription, and why? Answer: Transcription turns on; sugar X acts as an inducer, binding the repressor so it releases the operator and RNA polymerase can transcribe the genes.
2. In a made-up operon, transcription is high only when an activator protein is bound; there is no repressor. If the activator cannot bind DNA, is this loss of positive or negative control, and what is the transcription level? Answer: Loss of positive control; transcription is low or absent because RNA polymerase rarely initiates without the activator.
3. A gene is amplified from 2 copies to 12 copies, and each copy makes 20 mRNAs per hour. If methylation silences 4 of the copies, how many mRNAs per hour does the cell make, and what is the fold change over the normal 40 mRNAs per hour? Answer: 8 active copies × 20 = 160 mRNAs per hour; 160 / 40 = 4×.
4. A cell loses one copy of a tumor suppressor gene and the remaining copy is overexpressed threefold. Is the brake likely lost? Answer: No. Tumor suppressors need loss of both copies; one remaining functional copy still provides the brake, and overexpression of it does not cause gain of function.
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