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Former Faculty

 

Dr. 
Joseph Martens

Photo of Dr. 
Martens

The Regulation of Gene Expression in Yeast
 
Assistant Professor
 
Dr. Martens received his Ph.D. in 1999 with Chris Brandl at the University of Western Ontario, performed his postdoctoral studies with Fred Winston at Harvard University, and joined the Department in 2005.

Currently, Dr. Martens is accepting graduate students in his laboratory. Dr. Martens is accepting undergraduate researchers, and does sponsor students in other laboratories.

Professional Interests - Publications - Contact Information - Lab Personnel

Professional Interests of Joseph Martens

Figure 1
Figure 1. A model for SER3 regulation by transcription of intergenic non-protein-coding DNA (ncDNA). SER3 encodes and enzyme required for serine biosynthesis. Transcription of SER3 is repressed when cells are grown in media containing serine and is activated when cells are grown in media lacking serine. The serine-dependent expression of SER3 is controlled by a unique transcription interference mechanism that involves the transcription of adjacent intergenic ncDNA, which we termed SRG1 (SER3 Repressor Gene 1). In high serine concentrations, the Cha4 activator binds to the SRG1 promoter and recruits SAGA and Swi/Snf chromatin modification complexes and together, these factors induce high levels of SRG1 transcription. SRG1 transcription across the SER3 promoter interferes with the binding of transcription activators and results in SER3 repression. Under serine-starvation conditions, Cha4 is no longer able to recruit SAGA and Swi/Snf, resulting in decreased SRG1 transcription, which allows activators (Act) to bind the SER3 promoter and induce SER3 expression.

Normal cell growth and development is dependent on a dynamic gene expression program where genes are turned on when they are needed and turned off when they are no longer required. Failure to maintain proper control of gene expression can lead to cell death or uncontrolled cell growth; two fates that often are at the root of many human diseases and cancers. Eukaryotic gene expression is a complex process that is regulated at multiple levels, including the initiation, elongation and termination of transcription, the stability of the mRNA transcripts, and the translation of mRNAs into proteins. Research in our lab focuses on understanding the molecular mechanisms that are involved in controlling gene expression in the budding yeast, Saccharomyces cerevisiae. S. cerevisiae has proven to be an excellent model organism because many of the factors and mechanisms that are known to regulate gene expression and other cellular processes are highly conserved with larger eukaryotes including humans. We employ all of the tools available in yeast, including classical and molecular genetics, molecular biology, genomics and biochemistry to study several important aspects of gene regulation.

Analysis of intergenic transcription and its roles in yeast gene expression.

Our understanding of the control of gene expression has been primarily based on studies that identified and characterized protein factors that play diverse roles in these processes. However, it is becoming increasingly clear that, in addition to these proteins, the transcription of non-protein-coding DNA (ncDNA) can have profound effects on the regulation of gene expression. Several studies have implicated either transcription of ncDNA or its ncRNA product in controlling chromosome architecture, mRNA turnover, translation, and transcription initiation. However, the importance of transcription from ncDNA has not been fully appreciated until recent whole-genome expression studies revealed that transcription of ncDNA is the dominant genomic output of many eukaryotic organisms, including yeast and human. Based on the volume of this transcriptional activity, it is likely that we are only beginning to understand the importance of this largely ignored region of the genome.

In S. cerevisiae, we have recently uncovered a previously uncharacterized mechanism of gene repression that involves transcription of ncDNA (Figure 1). What is unique about this mechanism is that the ncRNA product is not required for repression, rather it is the act of transcribing the ncDNA that represses the adjacent protein-coding gene by interfering with the binding of transcriptional activators. Using these studies as our foundation, we continue to investigate the impact of intergenic transcription on gene expression. Current research activities include:

 
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