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UO / Biology / BIO 320 / Why are immediate early genes important?

Why are immediate early genes important?

Why are immediate early genes important?

Description

School: University of Oregon
Department: Biology
Course: Molecular Genetics
Professor: Jana prykril
Term: Fall 2016
Tags:
Cost: 50
Name: Mol Gen Midterm one study sheet
Description: Good luck!
Uploaded: 10/27/2016
4 Pages 36 Views 1 Unlocks
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Come DNA damage (SOS)


Why are immediate early genes important?



NUS

study Soup

cleavage

* Deciding Between hyticthysogenic upon infection

* Phage a utilizes E. coli protiens. → # of Viral Particles /cell

→ RNA POL + 6

→ FISH

•High Moi=hysogen: how E. coli population

Lytic Induction 2


What are early and late genes?



→ 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


What is the function of late gene regulation?



DNA repair

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

proteolytec cleavage

NH

PR

Cros We also discuss several other topics like What food has the most vitamin b5?

AtR

tumus ou PR

turns on TX @ Pk

turus on PR

initiation stalls on - to mimic.

* Antiterminator

Q loads onto RNA POL RNA POL Holoenzyme in Abortive

Lois binding site QBE

Q located precisely @ promoter PR'

from DNA

by initiating Tx from

PRED

PRE

turnson PR

ogenic Don't forget about the age old question of What is structuralism according to levi strauss?

FASH Sacrifice

O

&

P

cl|| FtsH sacrifice

all

Turus on PAQ

tumus on

more t genome expressed.

PR

(no cap-more

Lytle)

Dearades

PT

Degrades

Lytic

High Moi Number of viral particles infecting a

Late genes

la to make a Q MR

FtsH (CAP J

Int genes

cell

study

Study Soup

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:

CIPRM

cc

NO DNA

Binding

* 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

Tetramerice

oup

~ 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°)

t-TX terminator

Imagined/real terminator

phage DNA replication proteins

Good promoters: PL, PR, PR"

lysis

Cos7

Stud

Study

PR →

→PRE

Promoters that need help: phage recombination

PRM, PREPAQ, PI proteins

proteins

for fromeI/PRN CI Activator

fromPR Antiterminators:

Ni works on tr, kl, ti

from PL excisionase xis

Q; works on ER Py 1. Immediate early genes cos

From PR Integase Int

N

cro

Repressors: from Ph from PR

Суб PRм, о стх (ау

Ar(CI) - PR+PL, PRM @ + [ar] 2. Delayed early genes tit

CMT

CII, Q.CO+P)

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

---> Crocro

Genes CIPRM CIP FASHTI & II

Pi

PRM PR PRE

LPI

Soup len

PLN? SIP

PL

PAQ

Recom.

H+ TI SE

) Study Soup

05 00382 to 8

88

ti

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

@ORY

YRCI

dy

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,...

protientinds

RNAPOL

63 -5RES JAG

U AGE 3' mRNA

- AAAS' Template so +1 KBS ATGIV ayadsyn TTT 3' coding

3'

SO

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.

Glucose

Adenylate cyclase → CAMP

CAP

TX

.

poudySoup

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

TXON:

tary

laca

-CAP Homodimer who

HT-Hmotif whent CAMP

Study soup

promoter

Arac

·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

PC

* Arac Activates PBAD + Blocks PC II O Ava Operon:

(C1) (961) lcc TXON:L Arak Arabwase Arato

KNAPOL Adhvation Domain

so

PC

Site TT

PBAD

o txp Operon O mRNA

sup

TXON: [p] * \ [trp"ERNA]

e trptep coddu over

+

*Ribosomestatted

plancuer1 III @ trptxp codon over 1

MRNA:

SO

1

2

LRB E D CBA

ONA -

RBS header

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.

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