Becom Block 2

OriC

Prokaryotic origin of replication rich in A=T

DNAa

prokaryotic replication- breaks hydrogen bond of the A=T rich region of the 13bp by rapping the 9bp

DNAb

is a helicase that uses ATP to break h-bonds to seperate strands

DNAc

Carries DNAb to the helix

Single strand binding protien (SSB)

keeps DNA in prokaryotes from reannealing during replication

DNA gyrase

(topoisomerase) prevents supercoiling by cutting DNA during prokaryotic replication

Floroquinolone

an antibiotic that targets DNA gyrase preventing the phosphodiester bond

Primase

Lays down RNA primer

DNA Pol. III

synthesizes leading and lagging strand in prokaryotes

DNA Pol. I

exonuclease activity- removes RNA primers

polymerase activity- adds nucleotides to the 3’ end

In prokaryotes

ARS(autonomously replicating sequences)

In eukaryotes meaning multiple origins of replication

ORC (origin recognition complex)

binds to origin DNA sequence in eukaryotes and recruits Cdc6 and Cdt1

Cdc6 and Cdt1

recruit helicase to unwind DNA in eukaryotic replication and are only produced in G1

DNA Pol E

adds nucleotides continuously in eukaryotes

DNA Pol. G

adds nucleotides via Okazaki fragments in eukaryotes

PCNA

functions as a sliding clamp for eukaryotic polymerase activity

Telomerase

Makes a 3’ overhang which forms a T-loop and is protected by shelterin

BER deamination

cytosine is converted to uracil and gives rise to A=T

BER damage from hydroxy radicals

hydroxy radicals convert G to 8oxoG which gives rise to more T=A

BER methylation

methylation of adenine blocks replication

Short patch pathway

for BER when only a single nucleotide needs to be fixed, uses PNKP, PARP, XRCCI, and DNA Pol Beta

Long patch pathway

for BER when multiple nucleotides need to be fixed, uses flap endonuclease, DNA Pol E and G

BER deficiency

MUTYH gene results in MAP, polyps forming corectal cancer

MMR deficeint

causes endometrial cancer and Lynch Syndrome

MMR repairs

tautomerization

deamination

slippage

MMR Pathway

uses MSH, MLH, Exo1, and DNA Pol. G

NER

recognize messed up double helix that arise from environmental insults like UV, pyrimidine dimers, or adducts

TC-NER

detected by stalling of RNA Pol during transcription

GG-NER

detected by stalling of RNA pol during replication

Deficiency in TC-NER

causes impared development, premature aging, and Cockayne syndrome

Deficincy in GG-NER

early onset cancer partially induced by UV or Xeroderma Pigmentosum

NHEJ

repairs double strand breaks in nondividing cells caused by ionizing radiation

gives rise to adaptive immune response

Mutation in ATM

gives rise to ataxia telangisctasia

HRR

repairs double stranded breaks in activly dividing cell but may cause loss of heterozygosity leads to increase chance of woman cancer

Transcription

1. Promotor recognition

2. transcription initiation

3. chein elongation

4. chain termination

Modification of mRNA

1. 5’ capping

2. polyadenylation of 3’ end

3. intron splicing

Bacterial ribosome

50S—23S+5S

30—16S

Eukaryotic ribosome

60S—28S+5.8S+5S

40S—18S

Rifampin

inhibits RNA synthesis

Stop codons

UAG, UAA, UGA

Start codon

AUG

Macrolades

Bind 50S unit and inhibit protein synthesis

Oxazolidinoses

bind P site of 50S unit

Aminoglycosides

bind 16S unit

Tetracyclins

inhibit tRNA from interacting with 30S unit and treats Lyme disease

Streptogramins

inhibit late stage protein synthesis via 23S

Transformation

uptake of DNA from environment

Transduction

transfer of DNA via virus

Botulimun toxin

Blocks Ach release—> floopy muscles

Tetanus toxin

Blocks GABA/glycine release—→spastic paralysis

Lincosamide and chloramphenicol

block P site of 50S ribosome