DNA Replication Flashcards
Basic Mechanism
DNA Helicase Unzips
Topoisomerase cuts
SSBs keep it apart
Primase creates primer
DNA Poly III synthesizes 5 to 3
DNA Poly I removes primer and makes it DNA
DNA Ligase puts together cut strands and Okasaki fragments
3 prime overhang
TTAGGG repeats in Telomeres
Telomerase fixes the problem by extending off an RNA template to create telomeres
Lagging Strand DNA Poly
Delta
Leading Strand DNA Poly
Epsilon
What phase does nucleotide synthesis begin
End of G1 (preparing for DNA synthesis)
Bulky adducts
Caused by benzopyrene getting oxidized and binding with guanine
Pyrimidine Dimers
formed by UV light
HNPCC (Lynch Syndrome)
Caused by problems in the mismatch repair pathway,
Increased risk for many types of cancers
Xeroderma pigmentosum
Mutations to the Nucleotide excision repair
Skin hypersensitive to sunlight
Highly susceptible to skin cancer
Acceptable Wobble base pairs
GU
IA
IC
IU
Prokaryote initiation of translation
30s subunit binds shine delgarno sequence upstream of AUG
IF1, IF2-GTP, IF3 bind
1 and 3 leave, GTP hydrolyzed
IF2 leaves and 70s binds to begin transcription
Eukaryotic initiation of translation
Cap of 5 primen binds EIFs and 40s ribosomal subunit
MRNA scanned for AUG within Kozak Sequence
Diptheria and EF2
His residue on eEF2 is covalently modified by diptherian toxin blocking translocation and preventing transcription
RNA Poly I
rRNA
RNA Poly II
mRNA and miRNA
RNA Poly III
tRNA and other small proteins
Binding of RNA transcription factors
TBP binds with coactivators to TATA box
TFIIA and TFIIB bind
TFIIF binds and gets RNA Polymerase to bind
TFIIE, TFIIH bind
5 prime methylguanosice
CAP placed onto DNA by phosphodiester linkages, not always attached to methionine
Stopping of eukaryotic transcription
AAUAAA sequence recognized
Signals for polyadenylation
Splicing of Introns
Recognition of GU AG sites U1 binds GU U2 binds A U1 meets up with U2 to form lasso Exons are ligated and lasso leaves with the Us
Components of tRNA
Dihydrouridine D loop Anticodon Loop Variable Loop Pseudouridine and ribothymidine in TPC loop CCA sequence at 3 prime end
Spinal Muscular Atrophy
Caused by mutation in SMN1 gene
Both copies must be mutated
Additional splice site removed due to C to T mutation causing hnRNP to be able to continue blocking splicing and binding of U1 and U2
G1 to S phase
CDK4/6 and Cyclin D
CDK2 and Cyclin E later
S phase
CDK2 and Cyclin A
G2 to M phase
CDK1 and Cyclin A/B
