Extensive research on plant-microbe interactions has revealed that microbes are necessary for plant health and development. However, little is known about the effect of plant-microbial interactions on seed germination. Seed dispersal via abiotic or biotic vectors exposes seeds to entirely new communities of microbes. Since seeds travel different dispersal distances, they are exposed to varying microbial communities. To understand how dispersal distance and microbial communities interact to affect seed germination, I plan to germinate 12 native and invasive California grassland plant species under local versus foreign microbial conditions. The local microbial condition will consist of soil microbes collected from the McLaughlin Natural Reserve; a grassland plant community which the majority of plant species used in this study were collected from. Soil microbes collected from the Mojave Desert will be used as the foreign microbial condition in an attempt to determine how different microbial communities will affect grassland plant species. The Mojave Desert is outside the species’ ranges used in the study and is therefore likely to be the nearest foreign soil microbial community for all species. Species with shorter dispersal distances are expected to germinate at higher rates with local microbial communities since they are exposed to microbes near their origin site. Whereas, the germination of species with longer dispersal distances will be less affected by microbial origin since they experience broader exposure to microbial communities. This study will provide insight into critical plant-microbe interactions during the earliest stages of plant life.

The general topic of our research falls under molecular biology and genetics. The focus of our lab is studying genetic instability of microsatellite regions which are areas that have simple repeat sequences of DNA. For example trinucleotide (3 bases) or tetranucleotide (4 bases) bases in our genome. We care about this because it has been shown that the instability of CCTG tetranucleotide repeat sequences of DNA, can cause type 2 myotonic dystrophy. Some type 2 myotonic dystrophy patients have 1000's of CCTG repeats at a specific location. We are trying to understand the molecular mechanisms of how these repeats expand and thus further along the line perhaps we can apply the same principles to more complex organisms in efforts to contract these repeats helping us understand genetic diseases more. Our approach involves experimentation of our model organism Saccharomyces cerevisiae also known as budding yeast. We perform knockouts on genes of interest so that those genes are unable to be phenotypically expressed. With this technique, we aspire to figure out which genes in the yeast genome we hypothesize are involved in the contraction and expansion mutations that contribute to the genetic instability of these microsatellite regions.

The multicomponent mitochondrial coenzyme Q (CoQ) biosynthetic pathway is required to synthesize the ancient CoQ redox lipid, which is an essential electron carrier in the energy producing mitochondrial respiratory chain. Our lab revealed that components of the CoQ pathway assemble into distinct domains on the inner membrane, enriched at ER-mitochondria contact sites. We hypothesize that these assemblies facilitate substrate accessibility for efficient CoQ production and distribution. However, the way domains are regulated is not fully understood and the factors involved in regulation are unknown. To gain insight into maintenance and regulation of CoQ domains in cells, we conducted high throughput high-content imaging screen using genome-wide budding yeast deletion library expressing fluorescent markers for CoQ domains and mitochondria. We classified mutant phenotypes based on their deviation from wildtype and identified potential regulators of CoQ domains. These data will ultimately allow to explore the factors involved in the mechanisms that regulate CoQ domains in cells.

An activation domain (AD) is a part of a transcription factor (TF) that is responsible for increasing the probability of a gene being transcribed from DNA to mRNA. This is vital for subsequent production of specific proteins that make up the human body. Despite many activation domains having the same function, they are poorly understood because of their lack of sequence conservation and intrinsic disorder. Gcn4 and Gal4 are critical transcription factors in Saccharomyces cerevisiae for amino acid biosynthesis and galactose metabolism, respectively. Previous work has identified hydrophobic and acidic amino acid residues that contribute to activation domain function of these TFs. We searched 207 other yeast genomes for orthologs of Gcn4, identifying 502 unique proteins. Our preliminary work indicates that activation domains are much less conserved than DNA-binding domains. Alignments of these orthologs show that some, but not all, of the hydrophobic residues important for activity are conserved. The acidic amino acids glutamate and aspartate were not well conserved, but we found evidence that they convert into each other near important hydrophobic motifs. Even though these acidic residues are not conserved, the negative charge characteristic is conserved. Thus, this work shows how structural constraints shape the evolution of the Gcn4 activation domains. This work will enhance our understanding of how TFs regulate gene expression and how ADs function despite their poor sequence conservation, allowing scientists to combat TF-based diseases such as certain forms of diabetes and cancer.