chapter 16: the molecular basis of inheritance

double helix

double helix

the structure of DNA formed by double strands

mismatch repair

repair enzymes fixing errors in base-pairing

nuclease

enzyme that degrades nucleic acids

Frederick Griffith’s experiment and what he meant by “transformation”

• involved taking a pathogenic strain of DNA and seeing how it affected non-pathogenic DNA strands. It showed the pathogenic strands would turn the harmless ones into pathogenic

• proved that something can cause DNA to change

Avery and his colleagues discovery

• proved DNA is material used in transformation

• shows DNA is what caused harmless strains becoming pathogenic

bacteriophage

virus that infects bacteria

hershey and chase experiment

• labeled the protein and DNA of a bacteriophage radioactively in separate tests. later bleneded the phage and bacteria to separate into protein layer and “organic pellet”

• when protein was labeled, radiation would be in protein layer. when DNA labeled, it was in the “organic pellet” meaning that is what transferred into the bacteria

• proved DNA is genetic material

erwin chargaff’s discovery

[A] = [T]

[C] = [G]

rosalind franklin discovery with DNA structure

took a picture of DNA structure using DNA crystallography and proved it was a double helix

watson and crick

discovered DNA ran antiparallel and it consists of purine bonded to a pyrimidine

3 proposed models of DNA replication

• conservative: of the 2 daughter cells, one gets the original strand and the other gets brand-new strand

• semi-conservative: the original DNA strand is copied in a way that each daughter cells gets 1 new strand and 1 original strand

• dispersive: different sections of DNA is received by daughter cells, part of each strand being new and old.

meselson and stahl experiment and what it proved

• used different isotopes of nitrogen, which all are different weights, to label the original strand of DNA and new strands in a way to make them separate

• proved that after several generations, the DNA replicated in a way that the semi-conservative model is correct model

replication fork

“bubble” in DNA strand where replication is occurring

function of helicase

it breaks the double-helix to allow for the replication fork to open

function of single-strand DNA binding proteins

support the separated single-DNA strands until they can be copied

primer and why it’s necessary

initial sequence of RNA nucleotides used to initiate DNA replication

primase

places down the primer because it can start a RNA strand from scratch

DNA polymerase

extend the primer and replaces primer RNA nucleotides with DNA ones

synthesis of lagging strand vs leading strand

• leading strand can be done continuously because it is in the direction of the fork

• lagging strand is done in discontinuous fragments because it is being synthesized away from fork opening

okazaki fragment

unconnected DNA fragments of lagging strand

function of DNA ligase

used to stitch together Okazaki fragments

length of DNA as it undergoes more and more replication

it slowly gets shorter and shorter because when the primer gets removed, there is no 5’ end for the polymerase to add onto

telomeres

repeating segments of nucleotides at end of chromosomes to prevent them from getting too short too fast

telomerase

• lengthens the telomeres in germ cells

• found in somatic cancer cells because it lets them be capable of unlimited division