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NBME 20 Answers

nbme20/Block 1/Question#11 (38.5 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(884),
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sA seirdbdce in het equstion es,tm thsi mntoauit ucsorc wnihit an nrinto (a gene etenmsg ichhw si rabetnsdric DAN-;][gANt&R ubt ont )tladarnse.t NAR pcsilgni es)zeymn( grba RNA dna pool“ it;” an inotrn is tcu tou dna eht eoxns no hterie seid fo het tiornn are nded,oiaj leki i:hts

o1teoinx—2x—ronnne t=;g& 12oxenexn—o

a,pcyylliT tsih lciingps cursoc ta het veyr deges fo the onrtin thwa( I etdendo tiwh hte ”—“ ).hatreracc utB ni uro ,eacs a umntitoa tiwnih hte oinrtn is inuagsc ANR psiniglc yneemz to crnzogeei a new t:sei teh pceslir sutc nithwi teh rntnio sda(tien fo at het eryv d,gee as it ouhs.ld) oS, ew tge gteoisnhm htat lokso kile :this

oontnxee—12—xnri

atT’sh a yttallo nedftfeir NAmR olleu,cme dan i'ts niggo ot kmae our l-nbgoiβ petrino kolo nad( hv)eabe llywfua restga.n

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 +4  
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. +  



 +3 
submitted by monoloco(136),
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siTh ahs to od tihw ontirn icpisng.l bermeemR TA.GG siTh iuttaonm dinduec na AG eolscr eherw ti was spoupesd ot ,eb so semo fo htat ntroni tjus eacebm na neox.




 +3 
submitted by waterloo(74),

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.