RNA biology lecture 6 Flashcards

1
Q

Cap snatching by influenza

A
  • Capping confers stability + ensures export from nucleus
  • Depends on RNAPII
  • Creates issue for virus which transcribe host DNA w/ own polymerase as lack CTD
  • RNA virus often replicate in cytoplasm, use cells capping machinery
  • Influenza virus = in nucleus, x have CTD, steals cap form emerging pre-mRNA w/ endoribonuc acclivity
  • Cap is used as a primer to initiate transcription of its own RNA
  • Viral RNA then capped so protected from 5’-3’ degradation + exported to cytoplasm
  • Host RNA x have cap, vulnerable to nucleases
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2
Q

Capping, early checkpoint release + disease

A
  • Protein encoded by herpes simplex virus inhibits action of CDK9, prevents phosph of Ser 2
  • Pol stalls at early checkpoint + x released, host transcripts suppressed
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3
Q

Mutations that affect pre-mRNA processing

A
  • Mutations often found in regions needed for processing machinery to assoc w/ pre-mRNA e.g. 5’SS, ESE, 3’SS
  • Mutation affecting splice site → ↓ splicing of exons + faulty mRNA
  • Mutation in polyA signal ↓ or ↑ cleavage + poly adenyl
  • 2 types of mutation: 1. splicing mutation that directly effect consensus signal cause exon skipping, 2. mutation that affect trans-factor so impair splicing machinery
  • E.g. fontrotemporal dementia has mutations in MAPT genes
    E,g, Tau enriched in axons, Tau3/4 ration is highly regulated, deviation → accumulation of Tau → neuroses.
  • E.g. DMD caused by deletions + mutations e.g. T→A sub in exon 31 that creates an ESS forces exon31 skipping
  • Mutation in cis-elements: can promote cancer initiation + progression e.g. KIT oncogene
  • Mutation in splicing factors:
  • E.g. PWS = ↑ symptoms like restricted growth
  • Deletion of paternal SNURF-SnRNP causes PWS by loss of snoRNA, SnoRNA HB11=S2 comp to 5HT2CR pre-mRNA
  • PWS = mutation in 5HT2CR, deletion in chromosome 15 that encodes snoRNA inc SNORD115
  • SNORD115 assoc w/ exon 5 + suppresses activation of 5a splice site
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4
Q

Mis-splicing in cancer

A
  • No. of mutations that inactivate splice sites either directly or indirectly by affecting splice regulatory sequencing
  • Mutations to spliceosome e.g. U2AF
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5
Q

3’ end formation + disease

A
  • Largely occur in essential cis-elements, leads to Low or Gof
  • E.g. thalassemia due to mutation in AATAAA hexamer (recognition signal needed for interaction of CPSF w/ pre-mRNA)
  • Mutation in B globin gene Δ hexamer so CPSF x recognise → ↓ B globin protein → aggregation
  • Mutation in coagulation factor III where weak consensus site
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6
Q

Influenza A virus

A
  • Virus transcribes template, poly-adenyl occurs by transcribing U-rich region in template strand + repeatedly copying U-stretch → export
  • mRNA translated to make NS1 which assoc. w/ CPSF1
  • AAUAAA in pre-mRNA comprises host mRNA
  • NS1 also inhibits splicing by binding + inactivating u6 snRNP
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