Come DNA damage (SOS)
* Deciding Between hyticthysogenic upon infection
* Phage a utilizes E. coli protiens. → # of Viral Particles /cell
→ RNA POL + 6
•High Moi=hysogen: how E. coli population
Lytic Induction 2
→ Reca lots of catcu made from multiple a genomes so overcome Eftsh] from single E. coli genome If you want to learn more check out What is the meaning of social comparison theory?
and Co wins over Q → Growing conditious
• Happy cells = Lytic: Enouqu reasources for large E.colipopulation TLFISH Sin thriving cells ch] so Qwius
RecA stimulates LexA - * Imunity to second phage infection due to established
enzymes Prophage making cllar to +PR+ Ph of new infector
PL * Anti Terminator N If you want to learn more check out What does the structure of dna provide?
More RecA= Move clear plaque is binding site = Nut site
Anywhere between promoter terminator being effected → Palandromic : EMSA Gelshift shows N If you want to learn more check out How do you use mo theory?
Blocks PRM binds to RNA not ONA
BlockS PL *Nattaches to mRNA 2 Structure while RNAPOL is Txing
Represses PR ?RNA POL must Tx Out for success Traus "Nus protieus made by
Activates E. coli assist N to attach to RNA POL to TX through terminator
Cros We also discuss several other topics like What food has the most vitamin b5?
tumus ou PR
turns on TX @ Pk
turus on PR
initiation stalls on - to mimic.
Q loads onto RNA POL RNA POL Holoenzyme in Abortive
Lois binding site QBE
Q located precisely @ promoter PR'
by initiating Tx from
ogenic Don't forget about the age old question of What is structuralism according to levi strauss?
cl|| FtsH sacrifice
Turus on PAQ
more t genome expressed.
High Moi Number of viral particles infecting a
la to make a Q MR
FtsH (CAP J
мое лукома express
ar monomer Domains: Dimerice Activation
*To integrate Aphage DNA PLAN PRite el PRET We also discuss several other topics like What is the meaning of diaspora in colonial africa?
(low [FASHI) & To remaina stable phrophge:
* Expression of "int" from PL w/ Nyti
begets extralong mRNA targeted for destruction * Expression of "int" from Pitch w/ tit2 Pi
begets mRNA that is stable
~ 50 genes grouped into operous
"A regulatory & A structural gene region *Th control of cl
MRNA Z structure temp. dependant (no TL @ 450 yes Th @ 32°)
phage DNA replication proteins
Good promoters: PL, PR, PR"
Promoters that need help: phage recombination
PRM, PREPAQ, PI proteins
for fromeI/PRN CI Activator
Ni works on tr, kl, ti
from PL excisionase xis
Q; works on ER Py 1. Immediate early genes cos
From PR Integase Int
Repressors: from Ph from PR
Суб PRм, о стх (ау
Ar(CI) - PR+PL, PRM @ + [ar] 2. Delayed early genes tit
head Activators: (through thw/N)
from PL Gfrom BR
genes 2v (CI) → PRM 9. Late genes (through to w/N)
Lysis. Head, & Tail
- РАа Early Cornes
From RR w/Q through the PLN 1th PR CroltR
PR Lysis, Head & Tail Genes PR → ItR
Ph Nithic II Recombinase Delayed Early
PR croIER:CII,+P, Q
tall genes NytRPR
PRM CIlar Lysogenic
PAQ QURNA Nyth 7 PL (II CITI FtsHCII
PREitRiCIlar CII Pi integrase enzymes Lytic
CI - PAQ - XQmRNA TQ → PRI QERPRI-Lysis CII PRECIar).
A Head / Tail
Genes CIPRM CIP FASHTI & II
PRM PR PRE
H+ TI SE
) Study Soup
05 00382 to 8
ar buds w/highest affinity @ ORI as Diner I cooperatively binds as tetramer@ OR,
PRM PR Icro when bound @ OR + ORA
PRM when bound@ R3
→ loop forms to cooperatively bind OL3: Mrlar
* * Cro buds w/ lughest affinity @ OR as a a Dimer
PRM when bound
ODNA Binding Protiens -sequence specificity -
Major Groove Binding → Larger physical Space + Base Pairs orient more H-bond
donors + receptors here "Intermolecular Interactions > Accesability. Shape, Surface properties (charge/ A-bonds)
• Combinatoryal Control - Both cist Trans Activatovs + Repressors
Regulation Depends on cell type, developement, environmental Cheuncals
• Autimoren → Mutation impairs function of own allele product as well as interfering with wt allele function
*Doucingut negative Sugests homo multimer function Direct physical interaction allows impairment: if all subunits must be wt for wt multimer function.
Does not suggest hypermorph, no direct interaction w/ WT needed to show hypermorph phenotype .
Null mutations better/deletious better in case of hoveo multimer VO o second site Supression mutatious suggest direct interaction since allele specific
mut. in A can compensate for allele specific mut. in B if both mutatious occur
in interaction Domain are complementary o Codominance Both alleles express full phenotype independantly +@same time, lo Haplo insufficient One wt allele not enough to give wT phenotype (X"x ")
tcross w/ *©4 = 50% X X + 50% Xx4 * see in heterozygote w/ Xa not xx* o Hypermorphic hess functional than wTsee in x-x- or X-
Xa ne -Cross w X X = 100% X X
• Reporter gene construct - To test a promotor, insert Knowngene in front
•Screen visual identify working promotor cells as blue, not functional P = white
B-Gal reporter gener protien degrades x-Gal-blue Selection Reporter gene is Antibiotic resistance, only cells w/functionall grow EMSA Gel Shif Does Protien bind to RNA (Northern) /DNACWouthern)?
→ lanes w/t (protien] should see more bands higher up o Footprint Assay what region of RNAIDNA does Protien bind
Treat w/ cuting enzyme look for gaps in bands - Binding in that regional Conseusus Sequencetrustation - evolutonarily conserved reqious imporhan't, prov.
wl ss notation
C-term in Peptide,...
63 -5RES JAG
U AGE 3' mRNA
- AAAS' Template so +1 KBS ATGIV ayadsyn TTT 3' coding
o TX Initiation to
→RNAPOL core binds & factor - Holoenzyme (sequence specific, nou processive) 1. Binds to dsDNA = closed complex Reversable, not stably bound untilopen dys 4 of 6 recognizes - 35 for a 2. melts as DNA open complex RNA Pol not coming off now
(1.11 of 6 sits in DNA slot, moves out of the way for open complex
(2 of a recognizes -10, helps melt dsDNA - 13. Abortive initiation >RNA POL Starts making RNA, blocked by 6, restarts, uses ATP, stalls
→ 39 of 6 Sits in RNA exit channel, weeds to move, gets destabilized 4. Promoter escape i elugation o unbluds, core RNA POL TX's away
* Multiple 6 factors exist guide RNA POL to diff promoters to Tx diff sets
of genes based on consensus) under diff conditions 6 to - vegitative
one gene can have a promoters for diffo, diff levels of TX under diff conditions.
Adenylate cyclase → CAMP
olac Operon: Arepressort
allolactose/1PG TOAP + CAMP oox
CAR Binding operator taca
Lacz ß Galactosidase
breaks down Lactose
side product is allolactose
hacy lactose permeash
-CAP Homodimer who
HT-Hmotif whent CAMP
·lacI mutatious: laci + lack overcome by wr (t mut dimerization Domain)
lacet super repressor, wont bind altolactosel: overcomes WIL
laci Dominant negative, wont bind DNA operator overcomes WT - Constitutive mutations: + IPT6/-IPTG Always & Glucose
operater - ☆ cus laci → Traus Ressesive * Genetic Redundancy ORLOR, +OR3 - cause looping
lacto & Traus Dominant
• Uninducable Mutatious
*Repression loop CAR- Traus Dom
only wabibits PBAPTY Promoter as
PBAD PC can still Tx'a lac Is Trans Dom RNA POL/6 Tvaus Ress
Routledred foot preet CAP Binding site is
* Arac Activates PBAD + Blocks PC II O Ava Operon:
(C1) (961) lcc TXON:L Arak Arabwase Arato
KNAPOL Adhvation Domain
o txp Operon O mRNA
TXON: [p] * \ [trp"ERNA]
e trptep coddu over
plancuer1 III @ trptxp codon over 1
LRB E D CBA
HTX OFF: (trolt ttctro-ERNAT Ribosome
Stalled@ STOP codon over
→ WT Hoghtre 4 WT Low tre
AtrpR Low tre AtrpR High tre Atv p R High trp Dela AtrpR Low tre mut2
ousame MRNA Coperous) Allows dat leve is protien expression Prom ORF'S
Allows to make less protien than [MRNAJ - Quick protien synthesis in responce tostinesti Translational Regulation Benefits
* Also no Tx when type binds operator OR
no Ribosome initiates th:1=2.