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MCM > Exam 2- Fxns and Dysfunction in Genomic Regulation > Flashcards

Exam 2- Fxns and Dysfunction in Genomic Regulation Flashcards

1
Q

Central dogma of molecular biology

A
  • DNA to RNA via transciption
  • RNA to protein via translation
  • DNA replication via mitosis
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2
Q

meiosis

A

-transfer of genetic information from parent to offspring

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3
Q

exclusive carrier of information from DNA to protein

A

mRNA

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4
Q

RNA virus

A
  • can be reverse transcribed into DNA using reverse transciptase
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5
Q

transcription vs translation

A
  • transcription is DNA to RNA (same language)

- translation if RNA to protein (different language)

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6
Q

structure of DNA

A
  • DNA is double stranded and antiparallel
  • strands connected by hydrogen bonds between nucleotides
  • strands are polar with a 5’ and 3’ end
  • sugar-phosphate backbone forms major and minor grooves
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7
Q

Hydrogen bonds between nucleotides

A
  • G to C has 3 H-bonds

- A to T has 2 H-bonds

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8
Q

importance of condensation of mitotic chromosomes

A
  • mitotic chromosomes are condensed to prevent physical damage to DNA when cells are separated and DNA is passed on to daughter cells
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9
Q

DNA packaging

A
  • DNA is wrapped around histone octamer using hydrogen bonds to form nucleosomes
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10
Q

Histone proteins

A
  • 20% of histone proteins AA residues are Lys or Arg (have NH+ group)
  • Lys and arg are targets of PTM
  • histone proteins are highly conserved across species
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11
Q

nucleosome

A
  • basic unit of chromosome packing

- each nucleosome core consists of a complex of 8 histone proteins

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12
Q

histone octamer

A
  • protein around which DNA is wound

- protein + DNA= chromatin

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13
Q

euchromatin

A
  • lightly packed form of chromatin
  • often under active transcription
  • most active part of genome
  • 92% of human genome is euchromatin
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14
Q

heterochromatin

A
  • very condensed chromatin
  • seemingly genetically inactive
  • highly concentrated at centromeres and telomeres
  • very few active genes, those that are presents are resistant to gene expression
  • position effect: activity of a gene depends on relative position on the chromosome
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15
Q

What information is found on chromosomes?

A

1) genes (encoding proteins and RNA molecules)

2) interspersed DNA that does not contain genes (regulatory information, “junk” DNA)

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16
Q

year watson and crick describe the double helical structure of DNA

A

1953

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17
Q

year nirenberg, khorana and holley determin the genetic code

A

1966

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18
Q

February 2001

A

the sequence of the human genome (human genome project) was announced, it was only 90% completed, finished in 2004

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19
Q

percentage of DNA sequence in exons (protein coding sequences)

A

1.5%

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20
Q

microRNA

A

1) precursor folds back on itself using H bonds
2) Dicer moves along double stranded RNA and cuts it into shorter segment
3) 1 strand of the small segments is degraded and the other associates with a complex of proteins
4) bound miRNA wan base-pair with any target mRNA that contains a complementary sequence
5) miRNA either induce degradation of mRNA or block translation of mRNA

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21
Q

Coding sequences of DNA and RNA

A
  • exons

- they are spliced together out of mRNA

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22
Q

Start/end sequences of introns

A

intron mRNA sequences start with GT and end with AG 99% of the time

23
Q

Histone deacetylation

A
  • actively represses gene expression

- deacetylated chromatin is very compact and transciptionally repressed

24
Q

Histone acetylation

A
  • actively promotes gene expression
  • acetylated chromatin is open and transciptionally active
  • mediated by binding of transcription factors
25
Q

nuclear receptor signaling

A
  • lipophilic ligands (cholesterol derivatives) pass through the PM and nuclear membrane to bind to the DNA and cause transciptional modifications
26
Q

Post translational modifications of histones

A
  • alter histone interactions with DNA and nuclear proteins
  • histone protein tails are the target of multiple PTMs
  • most PTM focus on lysine and arginine residues
27
Q

DNA methylation

A
  • methy groups added to DNA by methyl transferase
  • changes activity of DNA sequence
  • represses gene transcription when at promoter
28
Q

PTM phosphoylation

A

often occurs at serine or threonine residues

29
Q

CpG Islands and Methylation

A
  • CpG islands in promoter acquire abnormal hypermethylation
  • silences gene
  • can be inherited by daughter cells
30
Q

Hypomethylation

A
  • chromosomal instability

- loss of imprinting

31
Q

nucleoside analog inhibitors

A
  • DNA polymerase requires a primer with a free 3’ -OH to begin processing
  • nucleoside analog inhibitors lack a 3’ -OH group and act as drugs that inhibit DNA replication i.e. cytarabine, acyclovir for herpes virus, and AZT for HIV
32
Q

DNA replication is..

A
  • semiconservative
  • bi directional with replication fork
  • semi- discontinuous (continuous leading strand synthesis, discontinuous/segmented lagging strand synthesis)
33
Q

Okazaki fragments

A

segments of DNA from lagging strand during DNA synthesis

34
Q

DNA helicase

A
  • pries apart the helix/unwinds DNA during synthesis

- binds and hydrolyzes ATP

35
Q

Single-stranded DNA binding protein

A
  • binds cooperatively to exposed ssDNA
  • helps stabilize unwound DNA and straightens DNA
  • prevents formation of hairpins
36
Q

topoisomerase

A
  • relieves over-wound supercoils
  • like untangling old phone cord
  • pharmaceutical drugs that target/inhibit DNA topoisomerase are used as anti-cancer agents (harm integrity of genome- lead to apoptosis)
37
Q

DNA ligase

A

It has three general functions: It seals repairs in the DNA, it seals recombination fragments, and it connects Okazaki fragments

38
Q

DNA polymerase

A

are enzymes that create DNA molecules by assembling nucleotides, the building blocks of DNA.

39
Q

Ionizing radiation (x-rays)

A

can damage DNA by:

  • DNA strand breaks
  • chemical modification of bases
  • DNA and proteins form cross-links
40
Q

nonionizing radiation (UV light)

A
  • can create pyrimidine dimers or 6-4 cross linkages between 2 pyrimidines (thymine dimers)
41
Q

spontaneous DNA damage

A
  • caused by endogenous agents
    1) depurination of Adenosine and guanine by removal of their bases (hydrolysis of N-glycosyl linkage)
    2) deamination of adenine/guanine/cytosine to generate hypoxanthine/xanthine/uracil
  • can result in base deletion or substitution
42
Q

Thymine modifications

A
  • formation of thymine dimers

- 6’-4’ covalent linkages of thymine bases

43
Q

intercalation

A

substance inserts itself in between DNA bases and damages DNA (thalidomide)

44
Q

direct repair

A
  • enzymatic repair

- damage repaired: pyrimidine dimers, O6-methylguanine

45
Q

base excision repair (BER)

A

Damage repaired: single-base mismatches, nondistorting alterations (i.e depurination)

46
Q

nucleotide excision repair (NER)

A
  • damage repaired: chemical adducts that distort DNA( pyrimidine dimers, BPDE-guanine adducts, cisplatin adducts)
  • associated disorder: Xeroderma pigmentosum
47
Q

mismatch excision repair (MER)

A
  • damage repaired: mismatched base in daughter strand

- associated disorder: Hereditary nonpolyposis colorectal cancers

48
Q

recombination repair/ homologous recombination

A
  • damage repaired: double-strand breaks, interstrand cross-linking
  • associated disorder: BRCA 1/2 breast cancer
49
Q

transcription coupled repair (TCR)

A
  • damage repaired: stalled RNA polymerase during transcription (not replication)
  • associated disorder: Cockayne syndrome
50
Q

Xeroderma pigmentosum

A

phenotype: skin CA, UV sensitivity, neurological abnormalities
process affected: nucleotide excision repair

51
Q

Hereditary nonpolyposis colorectal cancer

A

process affected: mismatch repair

52
Q

Hereditary nonpolyposis colorectal cancer

A

process affected: mismatch repair

-inherited in an autosomal dominant manor

53
Q

cockayne syndrome

A

Phenotype: developmental and neurological delay, photosensitivity, and progeria
process affected: transciption coupled repair
- if DNA is not repaired then this leads to early cell death

54
Q

BRCA associated breast CA

A

phenotype: breast, ovarian and prostate CA
process affected: repair by homologous recombination
- BRCA genes are tumor suppressor genes

MCM (5 decks)

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