Regulation of Gene Expression Flashcards

1
Q

Why regulate gene expression?

A

Waste of energy + no cell differentiation.

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2
Q

Proks and unicellular euks

A

Have to be able to respond to environmental cues:
-pH
-gases
-cell communication
-Presence or absence of food
-Temperature

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3
Q

Multicellular Euks Regulation

A

Have more ways of gene regulation than proks, and even unicellular euks.
-Same environmental cues
-Developmental changes: Fetal hemoglobin vs adult hemoglobin
-Cell specialization/differentiation: Pepsinogen - gene is in toes/liver, but only stomach expresses.

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4
Q

Sites of Gene regulation

A

-Transcription
-Post-transcriptional regulation
-Post-translational regulation

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5
Q

Transcription Regulation

A

DNA PHOSPHORYLATION ???Most modification occurs here, beginning of gene production.
-Chromatin modification (Epigenetic regulation?): DNA methylation (tighter) and Histone (protein) acetylation (looser).
-Transcription initiation: A key control point.

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6
Q

Post-transcriptional Regulation

A

-Alternative RNA splicing: 2 types of mRNA from a single hnRNA strand.
-mRNA degradation: Destroying mRNA depending on if you need it or not.
-mRNA location/availability: In Nucleus = can’t be translated

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7
Q

Post Translational Regulation

A

Regulation of protein activity

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8
Q

Constitutive Enzymes

A

Always there, i.e. glycolysis
-Most of bacterial enzymes, varies by cell type for multicellular euks.
-Might not last forever, but need them, so they make new ones.

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9
Q

Regulated Enzymes

A

On or off as needed.
-Digestive or Biosynthetic pathways:
-Fewer of bacterial enzymes, varies by cell type for multicellular euks.
-Some proteins during mitosis/meiosis, i.e. cyclins.

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10
Q

Operon

A

An operon is a collection of several genes for ONE biosynthetic pathway. Plus its regulatory regions.

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11
Q

Regulatory Regions

A

-Promoter: Site for RNA Polymerase.
-Operator: Controls access of RNA polymerase to genes. Repressor protein binding site.
-Activator Binding sites: Doesn’t have a cool name like promoter or operon.

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12
Q

Negative control vs. Positive control operons

A

Negative control: Use a repressor protein
Positive control: Use an activator protein.

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13
Q

Negative control operon

A

Use a repressor protein.
1. Repressible: Normally turned on (active). Corepressor binds to repressor, changes shape, and binds to operator. Blocking access of RNA Pol.
2. Inducible: Normally turned off. Inducer binds to repressor, repressor releases operator. Allowing access of RNA Pol.

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14
Q

Positive Control Operons

A

Use an activator protein.
1. Inducible: If [glucose] is low, then cAMP goes up, cAMP binds to CRP (cAMP Receptor Protein). CRP binds to DNA, increasing the transcription of lac operon (only possible if lactose has already bonded to receptor protein and removed it).

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15
Q

Proto-Oncogenes

A

Genes for normal cell growth and division.

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16
Q

Oncogenes

A

Cancer causing genes

17
Q

What causes a proto-oncogene to become an oncogene?

A
  1. Epigenetic changes: DNA Methylation and acetylation (Phosphorylation?)
  2. Translocation or transposition: Gene used to be under control of normal promoter, mutates, moved under a promoter that causes too many copies
  3. Gene amplification: Duplication of a region of a chromosome
  4. Point mutation: substitution, deletion/insertion.
18
Q

Tumor-Suppressor genes

A
  1. Normally prevent uncontrolled mitosis & growth
  2. Mutation here removes control, leads to cancer.
19
Q

Cell signaling pathway problems.

A
  1. Cell cycle-stimulating pathway:
    a. A protein stimulates cell cycle
    b. Cell cycle repeated too much -> cancer
  2. Cell cycle-inhibiting pathway defective:
    a. The protein that inhibits cell cycle not produced
    b. Uncontrolled cell cycle -> Cancer