Here's something I wrote when I was in college about my research. (You can't make this stuff up, kids.)

In eukaryotes, messenger RNAs (mRNAs) are edited via splicing before translation occurs. Small nuclear RNAs (snRNAs) associate with specific polypeptides to create small nuclear ribonucleoproteins (snRNPs). These snRNPs come together to form a multi snRNP complex called the spliceosome, the machinery of pre-mRNA splicing. Each snRNP is believed to be involved in recognition of certain nucleic acid sequences, helping to anchor the complex to the pre-mRNA, and ultimately help mediate RNA splicing. The affinity for the snRNAs to bind to the proteins and how the complex ultimately comes together are of interest to researchers, as structure often determines function. Any alteration to the formation of the complex will no doubt have a dramatic effect on the patterns of splicing. If this mechanism and the effects of mutation can be understood, then we will be one step closer to understanding how and why diseases caused by incorrect splicing occur.

My project involves the study of the pre-mRNA splicing mechanism in Drosophila melanogaster, the laboratory fruit fly. A mutagenesis screen will be carried out with a Drosophila strain, of my own creation, that has a mutant pre-mRNA splicing pattern. In this mutant, splicing out of the second intron is greatly reduced, and I would like to isolate modifiers of this gene I induce during mutagenesis. I will screen for the mutants first in vivo by looking for dominant eye color mutations, then isolate the mutation(s) by mapping the gene(s). Finally the gene(s) can be sequenced, and assessed for their role in affecting assembly of the spliceosome or suppression/activation of the U1 snRNP. Hopefully it will be possible in the future to take what we have learned about the genetics of the fruit fly, and apply our knowledge to the study of human diseases caused by pre-mRNA splicing defects to come up with more effective modes of treatment.