I. Operons – cluster of coordinately controlled
genes
A. Repressible
– gene turned off by excess end product
B. Inducible
– genes turned on only when compound present in environment
II. Lactose operon – inducible
A. Structural
genes on polycistronic mRNA
1. Z: beta-galactosidase; splits lactose into monosaccharides
2. Y: permease; moves lactose into cell
3. A: transferase; prevents breakdown of other disaccharides
B. Regulator
gene i
1. Different mRNA than operon
2. Repressor protein prevents transcription of operon
C. Operator
1. DNA where repressor binds
2. If repressor bound, no transcription
3. DNA sequence regions
a. O1 located at +11
b. O2 located at +412
c. O3 located at –82
d. tetramer of repressor binds to two of three regions at once
4. Tetramer of repressor binds to two of three regions at once
D. Induction
1. Repressor binds allolactose
2. Repressor changes shape
3. Repressor no longer binds DNA
4. Transcription occurs
E. Constitutive
mutants – always make beta-galactosidase
III. Catabolite repression – operons repressed
in presence of glucose
A. Absence of
glucose
1. CAP and cAMP bind promoter; CAP interacts with RNA polymerase
2. Binding enhances transcription
B. Presence of
glucose
1. No cAMP
2. No enhancement of transcription
IV. Tryptophan operon – repressible operon
A. Operator control
1. Repressor inactive
2. Repressor + corepressor (tryptophan) makes repressor active;
3. binds to DNA and prevents transcription
B. Attenuator
control
1. Leader transcript
a. Between operator and first gene
b. DNA of this region can form complementary loops
2. Leader peptide contains adjacent tryptophans
a. Excessive tryptophan - transcription of leader stops
b. Little or no tryptophan – transcription continues
3. Allows regulation based on availability of other amino acids
V. Phage lambda operons
A. Lytic cycle
– cro repressor favors these events
B. Lysogenic
cycle – cI repressor favors these events; integration requires site specific
recombination
C. Operons
1. Left, right; involved in DNA replication and integration
2. Late: phage heads, tails, lysis
D. Early and
late transcription
1. N and cro made
2. Allows transcription to continue through Q
3. Q allows late transcription
E. Repressor
transcription
1. cI, if made, binds to OL and OR
2. Duplication is inhibited
3. Repression prevents superinfection
F. Lysogeny vs.
lysis – binding of cI or cro
VI. Other transcription systems
A. Phage T4 –
early vs. late uses different sigma factors;
1. early uses host sigma; late uses phage products
B. Heat shock
proteins – promoters recognized by new sigma;
2. promoter sequence is CCCCATXT, not TATAAT
C. Promoter efficiency
– different sequences yield different efficiencies
VII. Translational control
A. Distance from
promoter on polycistronic mRNA
1. More ribosomes bound near 5' end
2. Destruction of mRNA from 3' end
B. Ribosome binding
efficiency depends on 5' sequence
VIII. Posttranslational control
A. Feedback inhibition
B. Protein degradation
1. N-terminal amino acid determines half-life; N-end rule
2. Regions rich in four amino acids (proline, glutamic acid, serine, threonine)
alter half-life:
a. PEST hypothesis
For questions, comments
and additional information, contact mfhicks@pstcc.edu
Last Updated: June 24
2001
Site map: Margaret
F. Hicks Home - Biology 2120 -
Notes
- Prokaryotic Gene Regulation
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