Lecture 17 Flashcards
(29 cards)
Similarities between prokaryotic and eukaryotic
Need to regulate initiation where whole genome replicated once, bidirection with rep fork, primase lays RNA primers at 3’OH, highly processive polymerase adds nucleotides 3’-5’ before dissociating, leading and lagging strand.
Control of division
E.Coli divides if given the right media + nutrients. Eukaryotic cells divide if there are signals that tell them to do so.
G1
Cells decide whether to divide or not. If not goes to G0. Cells can go between G1 and G0. But, once they pass restriction point, they must divide.
S
DNA synthesis. All DNA copied.
G2
Protein synthesis
M
Mitosis where daughter cells made
Progression through cell cycle
cyclins and cyclin-dependent protein kinases (CDKs) regulate cell cycle. Levels change during the cycle affecting kinase activity and that drives progression through cell cycle. Active CDKs phosphorylate cycle-involved proteins
G0
Most cells aren’t dividing. As we age, % G0 Cells increase. Different cells divide at different cells.
Senescent cells
Cannot reenter cell cycle
Quiescent cells
Cells that can be induced to enter cell cycle via mitotic signal
C1-S check
Checks for DNA damage. If there is damage, proteins can signal to the cell to not divide. If DNA is good, the protein won’t send signals. The proteins are phosphorylated by CDPK if there is DNA damage.
S-G2 check
Check for DNA damage and DNA synthesis is complete (no Okazaki fragments)
Importance of checks
once a cell goes through the cycle, the errors will be copied therefore checks are important
M check
Check sister chromatids are attached correctly to spindles before dividing
Oncogenes
Proto-oncogenes may accelerate division. When mutated, become oncogenes (dominant) as cells rapidly divide from cancer
Tumor suppressed genes
Slow division or induce apoptosis. Recessive mutation.
DNA changes and cancer
Mutations may be inherited or acquired (behaviours, randomly in c.c) e.g retinoblastoma proteins is a tumour suppressor protein. Dominant mutation is retinoblastoma. Increase risk in lung cancer.
Differences in pro and euk DNA polymerase alpha/primase
In prol, no proofreading and low processivity, lay down RNA primase beginning synthesis.
G1 phase
Cells select which origins to use. Pre-replicative complexes assembles.
Differences in pro and euk DNA polymerase sigma
Highly processive, proofreading. Equ. to DNA polymerase III. More packaging for Euk., multiple chromosomes (increases origin points for replication). In euk, not all of them activated during replication but all copied.
Synthesis
Active CDPK phosphorylate and activate pre-RCs. DNA polymerase recruited to copy DNA. Cluster of 20-80 sites initiated at a time. CDPKs inhibit pre-RC formation if replication occurred.
Repackaging
DNA needs to be repackaged in euk. if it is wrapped around histones which may be recycled or synthesised. Synthesis of histones is controlled at transcriptional and post transcription levels
Histones
Want it to happen at the correct time. Many copies of histone genes (most proteins have 1) allowing quick transcription. No introns therefore, don’t need to splice. Histone mRNA NOT polyadenylated (no tail of A at the ends) as it is quickly degraded once used. In E.Coli, supercoiling = repackaging.
Telomeres
End of chromosome. Repeating sequence 5’-TTAGGG-3’ which protects important information. Can be very long. Double stranded except where 3’ end extends off 5’ end.
