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NBME 20 Answers

nbme20/Block 1/Question#11 (40.6 difficulty score)
The sequence surrounding the first two exons ...
Disruption of normal splicing by creation of a new 3′ splice site🔍,📺
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 +16 
submitted by drdoom(957),
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As debrdesic ni eht ituqseno mets, tsih ttinmauo ruoccs wiihtn an nortin (a egen gemsent hiwch si erdrnactisb -]NN[gARtA;D& utb ont ls.rdettaa)n ANR gisilcnp (ee)yznms gbra NAR and pl“oo it”; an ntoinr si tuc uot dna eth esonx on iheert edsi of het ntrion ear jodenad,i ilek ht:si

1xnnieort—oxn2e—no &=tg; xe12n—xeono

cpilyay,Tl hist gsicinpl osrccu at hte yrve dseeg of eht notirn ah(wt I eondted whit teh ”—“ actrh.ac)re But in uor ec,as a itmtuano ihitwn hte troinn is sguican ARN cpsniigl zemney to iecznoreg a wen tes:i het licersp ctus nhiwti eth niornt dnsie(at of at the vrey e,gde as ti )lhodsu. o,S ew tge oihtegsmn thta oloks keli hst:i

onno1x—2xn—ereit

sT’tah a tloltya findteref AmNR lcm,eouel dan tis' goign ot keam uor nobgiβl- nieprto kool (and aeehb)v flywalu .tanrsge

drdanielr  I remember that in the pre-mRNA, the splicing sites of the intron where the spliceosome attaches are surrounded by "GU---AG" like "guac", so here the homologous DNA to this strand would be transcribed into "gu............ag......" and this would create a 3' slice site too soon +5  
vivarin  if this is supposed to be pre-mRNA, why are there T's in the sequence? I'm so confused by this for some reason +8  
sars  This is the gene (DNA), not heterogenous mRNA. +  



 +4 
submitted by monoloco(141),
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hiTs hsa to do whti rtnion pl.isngic bmReeemr A.TGG hsTi attuomni udidnce na AG croels rwehe it swa esppusdo to ,be os moes fo atth rtnnoi jstu mceaeb na en.xo




 +3 
submitted by waterloo(89),

I interpreted "sequence surrounding first two exons of gene" - to mean they must be talking about introns. Three of the answer choices don't have much to do with introns.

  • missense mutation would have to be in the exon to cause change in amino acid.
  • polyadenylation is at the end of the mRNA
  • inhibition of replication is DNA

that may not be air tight, but helps narrow down. Also knowing some B-thalassemia is due to variants in abnormal splicing helps. (FA 2019 pg 43)




 +1 
submitted by s1khwitit(1),

also remember that B-thalassemia is due to point mutations in splice sites and promoter sequences (FA19 pg410). If you create a mutation in a splice site you will surely mess up the correct mRNA needed to make a functional B-globin protein. That is how I answered the question.