DNA mutation & repair

core BMS

[blank] examples of DNA damage include base deamination, apurinic/apyramidic sites, ROS from metabolism, and replication errors

endogenous

[blank] examples of DNA damage include ionizing radiation exposure, UV light, and chemicals

exogenous

bases in DNA can undergo [blank] catalyzed de-amination

water

water catalyzed de-amination can lead to errors during DNA [blank]

replication

removal of [blanks] can lead to the formation of apyramidic or apurinic (AP) sites

bases

AP sites lead to errors [before/during/after] DNA replication

after

8-oxoG is a common product of [blank] oxygen species damage to DNA

reactive

8-oxoG is a [blank] analog that can bind with adenine

guanine

mismatch of [blanks] include A-C as imino form and GT as enol form

bases

mismatched bases can lead to DNA [blank]

slippage

ionizing [blank] can create ROS and cause both double strand and single strand breaks (think of triangle)

radiation

[blank] exposure leads to the linkage of two pyrimidine bases

UV

chemical [blanks] can cause DNA damage leading to numerous possible complications

agents

[blanks] are heritable changes in the sequence of a genome

mutations

gene [blanks] happen at a single loci and can involve multiple bases

mutations

a type of gene mutation, base [blanks] can lead to missense and nonsense mutations

substitutions

insertions and deletions can lead to [blank] mutations

frameshift

mutations can also occur in non-[blank] sequences and alter gene expression

coding

gene mutations can lead to gain or loss of protein [blank]

function

chromosomal [blanks] involve segments of one or more chromosomes and include deletion, duplication, inversion, insertion, and translocation

aberrations

deletion, duplication, and inversion only involve [x] chromosome

one

translocation and insertion involve more than one [blank]

chromosome

germline mutations are [blank] while somatic mutations are not

heritable

DNA [blank] repair involves base mismatch and DNA slippage

mismatch

Muts heterodimer or Muts homologs in eukaryotes (MSH) search for [blanked] DNA

mismatched

MSH recruits MLH (MutL homolog), post meiotic segregation protein (PMS), RFC, and PCNA to [blank] the DNA

cut

exonuclease 1 (Exo 1) [blanks] part of DNA with mismatch and DNA polymerase resynthesizes DNA

removes

UV-induced pyrimidine dimers can be repaired by [blank] (only in prokaryotes and marsupials)

photolyases

O-alkylated DNA lesions are repaired directly by [blank]

alkyltransferases

base [blank] repair targets DNA lesions that do not significantly distort the DNA helix (deamination, oxidation, alkylation)

excision

[blanks] recognize damaged bases in base excision repair and creates an AP site

glycosylyses

AP [blank] activity cuts the strand at the AP site in base excision repair

endonuclease

DNA pol [blank] resynthesizes DNA and DNA ligase fuses DNA in short patches of base excision repair

beta

DNA pol beta and sometimes gamma/epsilon are involved in the [blank] path of base excision repair

long

in the long path of base excision repair, flap [blank] cuts the long flap to allow for ligation

endonuclease

severe defects in [blank] excision repair are lethal

base

[blank] excision repair targets bulky lesions and involve either the GG-NER or TC-NER pathways

nucleotide

in global genome NER, the XPC complex identifies a [blank] excision and recruits UV-DDB which recruits TFIIH

nucleotide

in [blank] coupled NER, stalled RNA polymerase recruits CSA and CSB which backs up RNA polymerase

transcription

TFIIH [blanks] the lesion and opens up helix

verifies

XPF-ERCC1 and [blank] excise the DNA which is repaired by DNA pol.

XPG

homologous [blank] repairs double-strand breaks using Brca1 as a mediator

recombination

BRCA loads [blank] protein which is a recombinase that helps assemble ssDNA and dissociates to allow synthesis

Rad51

non-homologous end joining repairs double strand breaks using Ku 70/80 as [blank] proteins

scaffold

DNA PKcs and enzymes such as Artemis are responsible for [blank] processing

end

[blank] IV or XRCC4 can rejoin the ends in non-homologous end joining repair

ligase

non-homologous end joining is error [blank] but homologous end joining can only occur during S and G2 of the cell cycle

prone

defective XP protein affects the [blank] excision repair pathway, leading to xeroderma pigmentosum

nucleotide