3rd Place

 

Brian Lue

The John Cooper School

Teacher: Martina Davies

 

 

Alternative splicing occurs between transcription and translation, encompassed by a broader process known as pre-mRNA processing. At this stage, small nuclear ribonucleoprotein particles form spliceosome complexes around splice sites denoted by the binding of splicing factors. These spliceosomes then bend and pinch off portions of RNA, producing the final mRNA ready for translation (Black, 2003). Splicing, therefore, serves two essential purposes to extricate noncoding intron segments and to combine multiple configurations of exons in order to produce different sequences of mRNAs. . .


. . . Another major factor of splicing regulation involves the structure of the pre-mRNA itself. Researchers have found that the variable structure of the pre-mRNA either prevents or promotes access to specific splicing sites. Additionally, it can centralize splicing signals in order to encourage splicing (Warf & Berglund, 2010). Folding and splicing do not occur at distinct and separate intervals either; in fact, transcription occurs while the structure of the pre-mRNA is determined and the protein regulators are recruited. . .


. . . Indeed, the ubiquity of alternative splicing has led to increased interest in its relation to numerous diseases. Recent studies have shown that abnormal mRNA splicing in cancerous cells may explain some of their aberrant behavior. One specific example involves the production of the enzyme DNMT3B, which catalyzes DNA methylation. Abnormal splice forms of DNMT3B with retained introns and misplaced promoters lead to atypical methylation patterns, which cause the uncontrollable cell growth characteristic of tumorous cells (Fackenthal & Godley, 2008).