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

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

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)

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.