BIO 351 Lecture Notes - Lecture 12: Small Nuclear Rna, Phosphodiester Bond, Snrnp
Mechanism of Splicing Objectives
1. Identify conserved sequences at intron borders (donor, acceptor)
− 5’ Splie Site = Doo Site = highly oseed seuee of AGGT o AGGU i RNA that aks the egiig of
splicing
− 3’ Splie Site = Aepto Site = highly oseed seuee of AGG that marks the end of splicing
2. Describe how splice sites are recognized and cut (snRNP, snRNA, phosphoester transfer)
− Overview requires 2 phosphoester transfers
− Actual splicing requires Small Nuclear Ribonuclear Proteins (snRNPs) which consists of a protein complex and
Small Nuclear RNA (snRNA)
find more resources at oneclass.com
find more resources at oneclass.com
Document Summary
Identify conserved sequences at intron borders (donor, acceptor) 5" spli(cid:272)e site = do(cid:374)o(cid:396) site = highly (cid:272)o(cid:374)se(cid:396)(cid:448)ed se(cid:395)ue(cid:374)(cid:272)e of aggt (cid:894)o(cid:396) aggu i(cid:374) rna(cid:895) that (cid:373)a(cid:396)ks the (cid:271)egi(cid:374)(cid:374)i(cid:374)g of splicing. 3" spli(cid:272)e site = a(cid:272)(cid:272)epto(cid:396) site = highly (cid:272)o(cid:374)se(cid:396)(cid:448)ed se(cid:395)ue(cid:374)(cid:272)e of agg that marks the end of splicing: describe how splice sites are recognized and cut (snrnp, snrna, phosphoester transfer) Actual splicing requires small nuclear ribonuclear proteins (snrnps) which consists of a protein complex and. Small nuclear rna (snrna: site genetic evidence to describe the basis of disorder associated with mis-splicing of introns. Case study of tazwana williams had a blood disorder called thalassemia. Thalassemia = disease associated with low levels of -globin protein in red blood cells (rbcs), leading to small and misshapen rbcs. Discovered that she received two different mutations from her heterozygous parents. Bt1 has a 2 bp deletion in the promoter sequence leading to reduced or absent transcription.
