1
DNA replication Nucleotides Ribonucleotides Phosphodiester bonds 5' to 3' strand cell cycle Double helix Base pair G1 phase S phase G2 phase carcinogen M phase deletion frameshift mutation helicase germ line mutation lagging strand leading strand methyl-directed mismatch repair ligase missense mutation Okazaki fragment mutagen replication fork nondisjunction RNA primer nonsense mutation semiconservative single-stranded binding proteins telomerase topoisomerase silent mutation somatic mutation translocation tumor-suppressor gene Random nature Lederberg Experiment mitosis Interphase cytokinesis G1, G2, and S Phase Cell growth replication of chromosomes Synthesis of proteins for mitosis End of Interphase mitosis and cytokinesis Nucleus splits M Phase begins Cell splits in 2 DNA replication occurs Adenine Guanine Cytosine Thymine Uracil Codon Anti-codon Seperates DNA strands 5' to 3' Moves in Prevents strands from re-joining replication occurs outwards origin of replication Where DNA replication begins Splits into 2 forks (bidirectional replication) Template Strand model for replication/one strand is always template Preserving one template minimizes mutations Mutations Mutations still occur Not caused by environment Resistance was present prior to addition of T1 bacteriophage one amino acid change different amino acid sequence can cause No effect mutation in cells of gametes mutation in non-gamete cells DNA repair systems Mutations sometimes fixed base pair mismatch fixed by removal of strand Direct Repair converted to correct structure abnormal nucleotide/base fixed by removal of strand changes to stop codon substitution can cause can cause can cause cancer oncogene overactive gene/leads to uncontrolled cell growth creates cancer preventing proteins cause mutation in increase chance of cancer cause abnormal cell growth apoptosis insufficient cell death nucleotide excision repair things that cause mutations Cancer cells are stuck in 2 strands in replication one of the strands the other strand direction of synthesis direction of synthesis multiple RNA primers added so fragments form undoes the tangling caused by helicase links the fragments covalent bond used by ligase Reiji and Tuneko Ozaki researchers who found Type of Type of Type of Type of Type of replaces in RNA complementary complementary Type of Type of Type of Type of complementary nucleotides a set of 3 nucleotides complementary to codon structure of finished DNA DNA polymerase synthesizes DNA synthesizes DNA primase needed before to synthesize RNA primers necessary so DNA polymerase has -OH (hydroxyl) group to bind to enzyme that prevents chromosome shortening part of chromosome attaches to another chromosome cells do not properly divide inversion change in direction of genes on chromosome

DNA Replication and Mutation Concept Map

Embed Size (px)

DESCRIPTION

Concept map

Citation preview

Page 1: DNA Replication and Mutation Concept Map

DNA replication

Nucleotides

Ribonucleotides

Phosphodiester bonds

5' to 3'

strand

cell cycle

Double helix

Base pair

G1 phase

S phase

G2 phase

carcinogen

M phase

deletion

frameshift mutation

helicase

germ line mutation

lagging strandleading strand

methyl-directed mismatch repair

ligase

missense mutation

Okazaki fragment

mutagen

replication fork

nondisjunction

RNA primer

nonsense mutation

semiconservative single-stranded binding proteins

telomerase

topoisomerase

silent mutation

somatic mutation

translocation

tumor-suppressor gene

Random nature

Lederberg Experiment

mitosis

Interphase

cytokinesis

G1, G2, and S Phase

Cell growth

replication of chromosomes Synthesis of proteins for mitosis

End of Interphase

mitosis and cytokinesis

Nucleus splits

M Phase begins

Cell splits in 2

DNA replication occurs

Adenine

Guanine

Cytosine

Thymine

Uracil

Codon

Anti-codon

Seperates DNA strands

5' to 3'Moves in

Prevents strands from re-joining

replication occurs outwards

origin of replication Where DNA replication begins

Splits into 2 forks (bidirectional replication)

Template Strand

model for replication/one strand is always template

Preserving one template minimizes mutations

MutationsMutations still occur

Not caused by environment

Resistance was present prior to addition of T1 bacteriophage

one amino acid change

different amino acid sequence

can cause

No effect

mutation in cells of gametesmutation in non-gamete cells

DNA repair systems

Mutations sometimes fixed

base pair mismatch fixed by removal of strand

Direct Repair

converted to correct structure

abnormal nucleotide/base fixed by removal of strand

changes to stop codon

substitution

can cause

can cause

can cause

cancer

oncogene

overactive gene/leads to uncontrolled cell growth

creates cancer preventing proteins

cause mutation in

increase chance of cancer

cause abnormal cell growth

apoptosis insufficient cell death

nucleotide excision repair

things that cause mutations

Cancer cells are stuck in

2 strands in replication

one of the strandsthe other strand

direction of synthesis

direction of synthesis multiple RNA primers added so fragments form

undoes the tangling caused by helicase

links the fragments

covalent bond used by ligase

Reiji and Tuneko Ozaki

researchers who found

Type of

Type of

Type of

Type of

Type of

replaces in RNA

complementarycomplementary

Type of

Type of Type ofType of

complementary nucleotides

a set of 3 nucleotides

complementary to codon

structure of finished DNA

DNA polymerase

synthesizes DNA

synthesizes DNA

primase

needed before to synthesize RNA primers

necessary so DNA polymerase has -OH (hydroxyl) group to bind to

enzyme that prevents chromosome shortening

part of chromosome attaches to another chromosome

cells do not properly divide

inversion

change in direction of genes on chromosome