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summary genetics chapter 11-15
summary chapter 11-15 DNA replication, transcription, translation and regulation
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Chapter 11 DNA replication11.1 Structural overview of DNA replication
Existing DNA strands act as templates for the synthesis of new strands
During the replication the complementary strands come apart and both serve as template strands.
The two newly made stands are the daughter strands.
Three different models were proposed to describe the end result of DNA
replication
Conservative model = both parental strands remain together, 3 new strands and the old one
Semiconservative model = parental strands separated and again separated, correct.
Dispersive model = segments of parental DNA and segments newly made
11.2 bacterial DNA replication: the format of 2 replication forks at
the origin of rep
Bacterial chromosomes contain a single origin of replication
The synthesis of new daughter strands is initiated within tie origin and is bidirectionally. Two
Replication is initiated by binding of DNAA proteins to the origin
In E. coli, the origin is named oriC. Three types of sequences are found: AT-region, DnaA box and
GATC methylation sites.
Replication begins with binding of DnaA proteins to DnaA boxes DnaA proteins also binds to
themselves other proteins, HU and IHF cause DNA to bend around the complex DNA separates
at the AT-region DNA helicase binds to origin, DNAC protein assists DNA helicase moves 5’ to
3’ and separates the strands on both sides of the origin. GATC methylation sites are involved in -
regulating replication. Methylated by Dam, replication does not occur again until methylation is
done.
11.3 Bacterial DNA replication: synthesis of new DNA stands
Several proteins are required for DNA replication at the replication fork
Separation of the strands results in positive supercoiling topoisomerase 2 travels in front of DNA
helicase and causes this. The replication requires single-strand binding proteins bind to strand o
DNA and prevent them from re-forming the double helix.
Primase synthesizes short strands of RNA RNA primers. In the leading strand the primer is made
at the origin, the lagging strand has multiple primers. DNA polymerase synthesizes the new DNA
strand, by using 5 proteins: 1, 2, 3, 4 and 5. 1 and 3 for normal replication. 2, 4 and 5 for repair.
3 consists of 10 subunits and is the most important. α-subunit catalyzes bond formation between
nucleotides. Pol 1 removes RNA primers and fills the vacant regions with DNA.
The enzyme is formed like a hand, via the catalytic site the dNTPs enter and bind to the template.
The synthesis of leading and lagging strands is distinctly different
The synthesis of the leading strand is continual, as it moves 5’ to 3’. In the lagging strand, primers
repeatedly initiate synthesis, this is discontinuous Okazaki fragments. To complete the synthesis
in the lagging strand removal of RNA primers, DNA synthesis in those places and attachment of
fragments. Primers are removed by DNA Pol1, exonuclease gaps filled in by DNA Pol 1 DNA
ligase forms covalent bond between Okazaki fragments.
,Certain enzymes involved in DNA replication bind to each other to form a
complex
DNA helicase and primase are bound = primosome. Primosome is associated with 2 DNA pol
holoenzymes replisome. Dimeric DNA polymerase = two DNA pols that move as unit during
replication, the lagging strand is looped
Replication is terminated when the replication forks meet at the
termination sequences
On the opposite side of oriC is a termination sequence. The termination utilization substance (Tus)
binds to ter sequences and stops the replication fork. T1 stops left to right, T2 right to left. But
replication usually stops when one fork is stopped and the other fork reached the stopped fork. DNA
ligase links daughter strands. Replication often results in two catenanes topoisomerase 2 makes
temporary break and rejoins them.
The isolation of mutants has been instrumental to our understanding of
DNA replication
The first used mutant was in the gene that encodes DNA Pol 1. If researchers want to identify loss-
of-function mutations in vital genes conditional mutants. A type of this is temperature-sensitive
mutant.
Bacterial cells are exposed to a mutagen that increases likelihood of mutations cells are plated
and incubated in permissive temperature they are separated into permissive and non permissive
temperatures. The ones unable to grow are mutants. When shifted to nonpermissive temperatures
certain mutants showed rapid arrest in DNA synthesis rapid stop mutations.
11.4 Bacterial DNA replication: chemistry and accuracy
DNA pol 3 is a processive enzyme that uses dNTPs
The dNTP first enters the catalytic site of DNA Pol 3 and binds to template strand (AT/GC) 3’ OH
reacts with the PO4 2- of incoming nucleotide PPi is released. The DNA pol is a processive
enzyme, that is why it works so fast.
The β-subunit (clamp protein) promotes association of holoenzyme with DNA. In the absence of the
β-subunit the DNA pol does not work as fast and falls of very easily.
The fidelity of DNA replication is ensured by three mechanisms
Per 100 million nucleotides 1 mistake is made. The fidelity is very high. 3 factors account for this:
Stability of base pairing The stability is very low between mis matches
Structure of active site of DNA Pol the active site of DNA pol catalyzes attachment of
nucleotides when the correct bases are located in the opposite strands
Proofreading DNA pol can identify mismatches and remove them with exonuclease 3’-5’
11.5 Eukaryotic DNA replication
Initiation occurs at multiple origins of replication on linear chromosomes
More origins are needed, because the chromosome is longer. Bidirectionally from many origins
during S phase. In yeast origins have been studied and called ARS elements. 50 bp, hight AT rate
and copy of ARS consensus sequence (ATTTAT(A/G)TTTA.
DNA replication requires assembly of prereplication complex (preRC) during G1. Part of this is
origin recognition complex (ORC) acts as first initiator of preRC assembly promotes binding of
Cdc6, Cdt1 and MCM helicase completes DNA replication licensing.
, As S phase approaches preRC is converted to active replication site by phosphorylation promotes
release of Cdc6, Cdt1 and ORC MCM helicase move in 3’ to 5’ and replication proceeds.
Eukaryotes have many different DNA polymerases
DNA polymerase α is the only eukaryotic polymerase that associates with primase to synthesize
short RNA-DNA primer The complex dissociates and is replaced by DNA pol δ or ε (δ for lagging, ε
for leading) = polymerase switch
β is involved in removing incorrect bases. Many pols are in category translesion-replicating
polymerase.
Flap endonuclease removes RNA primers during eukaryotic replication
Flap endonuclease removes small RNA flaps, DNA delta polymerase elongates okazaki fragment
until it bumps into RNA primer flap is formed endonuclease and DNA ligase seals the
fragments together. Flaps that are too long are removed by Dna2 nuclease/helicase.
Ends of eukaryotic chromosomes are replicated by telomerase
Telomeric sequence contains G and many T. DNA pol is unable to replicate 3’ end of DNA strands. A
primer can not be made upstream from this point, to prevent loss of genetic information additional
sequences are added to the ends of telomers telomerase recognizes sequences at the end of the
chromosome and synthesis repeats. Occurs in three phases:
Binding of telomerase contains protein subunits and RNA, TERC contains complementary
sequence which allows binding
Polymerization RNA forms a template for 6 nucleotides, catalyzed by TERT.
Translocation telomerase moves to new end of strand and attaches another 6
nucleotides. This cycle occurs many times.
Telomere length may play role in aging and cancer
Activity of telomerase decreases with aging. When telomeres are too short cells become senescent =
lose ability to divide. Cancer cells carry a mutation in the activity of telomerase, preventing telomere
shortening which prevents senescent.
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