Position: Graduate Student
Contact: lstroud@bio.fsu.edu
Education: Bachelor of Science in Biological Sciences, Florida State University
Research Interests:
The initial characterization of chr120 point mutation alleles.
Epigenetic modifications, including DNA methylation, are associated with changes in gene expression. Hypermethylation of promoter regions is associated with gene silencing while their hypomethylation is associated with gene expression. The Arabidopsis (Arabidopsis thaliana) morpheus' molecule1 (mom1) mutant exhibits a loss of transcriptional silencing without the loss of associated DNA methylation in the promoter region. Maize (Zea mays) Chr120 has been determined to be an ortholog of MOM1, but function of this protein in maize is not known. We acquired four maize lines with mutant chr120 alleles from TILLING (Targeting Induced Local Lesions IN Genomes) populations generated by EMS mutagenesis. The first TILLING allele (chr120-L646F) we studied exhibited an albino phenotype. We observed some evidence for lethality for two of the other alleles, while the third did not demonstrate evidence for lethality or albinism. As EMS mutagenesis generates multiple mutations, we also considered chr120-L646F plants having a second mutation in W11. The mutant allele of the tightly linked W11 has been previously shown to give an albino phenotype. Our complementation analysis has determined that W11 and Chr120 however are neither allelic nor there is a second mutation in W11 in the chr120-L646F background. Because of its orthology with MOM1, we hypothesized that Chr120 might be an epigenetic regulator of gene expression. We tested this hypothesis by studying the affects of homozygous chr120-L646F on the epigenetically, transcriptionally silenced B1 transgene (BTG). Our preliminary results indicate that chr120-L646F does not relieve silencing of BTG. Future research will focus on identifying the gene responsible for the albino phenotype, and determining its interaction with Chr120.