Chapter 16 - Molecular Basis of Inheritance Flashcards

1
Q

Proved Theory of DNA Replication

A

Semiconservative Model: Proposed that when a double helix replicates, each of the daughter molecules will have an original strand plus a new strand

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2
Q

Alternate Theories of DNA Replication proven to be false

A

Conservative Model: after 1 round of replication, parental strands are joined together and two new strands come together, therefore 1 daughter cell has original parental DNA and 1 daughter cell has new DNA

Dispersive model: parental and new strands break in different parts and enzymes fill in the gaps with the alternating DNA strand so after 1 round of replication, each daughter cell has mixed and matched pairs of new and parental DNA strands

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3
Q

Origin of Replication

A

a short stretch of DNA that has a specific sequence of nucleotides

- Proteins recognize this sequence, bind to it and open up the circular DNA sequence to separate the two strands
- DNA replication then proceeds in both directions until all is copied, in eukaryotes there are a few hundred replication bubbles speeding up the process
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4
Q

Replication Fork

A

a Y shaped region at the end of each replication bubble where the parental strands are being unwound by several enzymes
- This allows single strand binding proteins to bind to the unpaired strands to prevent them from re-paringT

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5
Q

Topoisomerase:

A

an enzyme that helps relieve strain caused by the untwisting of the double helix at the replication form by breaking, swiveling and rejoining DNA strands.

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6
Q

How a New DNA Strand is Synthesized

A
  • a DNA primer is synthesized by primase and binds to the unwound strands to start a complementary chain
  • DNA polymerase catalyzes the synthesis of the rest of the DNA copy by adding nucleotides
  • strands are formed in antiparallel directions as DNA is only added to the 3’ of a primer
  • They begin in the middle at the replication origin with forks on either end, with 2 DNA polymerase working concurrently, 1 starting in the middle and at the 3’ end of the template strand moving both from 5’ to 3’ end of the new strand.
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7
Q

Semi Discontinuous Model of DNA synthesis: Leading Strand

A

the new complementary DNA strand being synthesized along the template strand towards the replication fork(the strand elongating in the direction as to where the template strands were opened up)
- Only 1 primer is required to synthesize the whole leading strand
- Synthesized continuously compared to lagging
- Requires a primer, DNA polymerase III, helicase enzyme and an SSB protein

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8
Q

Semi discontinuous model of DNA synthesis: Lagging Strand

A

a discontinuously synthesized DNA strand that elongates by means of Okazaki Fragments in a 5’-3’ direction away from the replication fork.
- DNA polymerase 3 works along the template strand away from origin of replication and towards replication fork until it hits a primer where it falls of, before binding further back and repeating process(move in direction of arrows above but starting at middle arrow before working backwards)
- Each okazaki fragment requires separate primers
- DNA ligase joins adjacent Okazaki fragments together by

- Requires primase and RNA primers, DNA polymerase III and I, DNA ligase
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9
Q

Proteins used within DNA replication

A
  • Helicase: unwinds parental double helix at replication forks
    • Singe-strand binding protein: binds and stabilizes single stranded DNA
    • Topoisomerase: relieves overwinding strain ahead of replication forks by breaking, swiveling and rejoining DNA
    • Primase: synthesizes an RNA primer at the 5’ end of each strand(start)
    • DNA Polymerase 3: synthesizes new DNA strand off of template strand in 5’-3’ direction
    • DNA ligase: joins Okazaki fragments and
      • DNA Polymerase 1: removes primers in lagging strand and replaces with nucleotide sequences
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10
Q

Trombone Model to describe DNA replication Complex

A

two DNA polymerase molecules, one on each template strand, ‘reel in’ the parental DNA and extrude newly made DNA molecules with the lagging strand being looped back through the complex

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11
Q

Proofreading and repairing DNA

A
  • DNA polymerase proofread each nucleotide against its template as soon as it is covalently bonded
    • If it finds an incorrect one, nucleases removes the nucleotide and DNA polymerase resumes synthesis
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12
Q

Mismatch repair

A

other specific enzymes which remove and replace incorrectly paired nucleotides
- if not repaired, it leads to a mutation

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13
Q

Nucleotide Excision Repair

A

A segment of the strand containing the damage is cut out by a DNA nuclease, and the resulting gap is filled in by DNA polymerase, ligase and nucleotides using the undamaged strand as a template

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14
Q

Issue with Replicating ends of DNA Molecules

A
  • In eukaryotic organisms with Linear DNA strands, usual replication machinery cannot complete the 5’ ends of daughter DNA strands because there is no 3’ end of a preexisting
    • As a result, repeated rounds of replication produce shorter and shorter DNA molecules with uneven ends
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15
Q

Telomeres

A

the multiple repetitions of one short DNA sequence at the end of a chromosome molecule which protects the organisms genes from being eroded during successive rounds of DNA replication

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16
Q

Telomere function

A
  1. Specific proteins associated with telomeric DNA prevent the staggered ends of daughter molecules from activating the cells system for monitoring DNA damage(cell death)
    1. Acts as a buffer zone which provides protection against the organisms genes shortening and eroding over successive replications(over time as more replications correlates with older ages)
      Doesn’t prevent by merely postpone
17
Q

Process of Telemorase in Cells

A
  • Telomerase contains its own RNA molecule which acts like a template, binding to a complementary sequence on the normal length DNA template strand, artificially extending that strand
    • Creates a primer upstream of the shortened, newly made DNA strand and gives DNA polymerase a template to join complementary nucleotide pairs to lengthen the shortened strand
      • Not active in most human somatic cells
18
Q

Telomere functioning in cancer cells

A
  • Normal shortening of telomeres may protect against cancer as it limits the number of divisions the cell can undergo
    • Cells from large tumors have unusually short telomeres, which is normal since they replicate uncontrollable, over time leading to self-destruction
      • Telomerase activity is abnormally high in cancer cells, suggesting it stabilizes telomere length and allows cancer cells to persist
19
Q
A