Needhi Bhalla, Dept. of MCD Biology

The Bhalla lab is interested in the mechanisms that ensure that chromosomes segregate correctly during cell division, particularly in meiosis. During this specialized cell division, diploid cells give rise to haploid gametes, such as sperm and eggs, so that diploidy is restored by fertilization. Defects in meiosis can generate gametes and, therefore, embryos with the incorrect number of chromsomes. These aberrations in chromosome number, also referred to as aneuploidy, typically produce inviable embryos. It is estimated that 30% of human miscarriages are due to aneuploidy. In some cases, the presence of an extra copy of a chromosome can be tolerated by a human embryo but results in serious developmental disorders, such as Down and Klinefelters syndrome. [More]

Glenn Millhauser, Dept. of Chemistry and Biochemistry

Amy Ralston, Dept. MCD Biology

Jeremy Sanford , Dept. of MCD Biology

Accumulation of somatic mutations during our life history contributes to the stochastic nature of aging and plays a key role in the onset of disease. The focus of this project is to understand how mutations induce disease phenotypes, a question directly relevant to many aspects of aging research. Here we investigate the hypothesis that disease-causative point mutations induce aberrant processing of messenger RNA by disrupting the specificity of protein-RNA interactions. Our first step towards elucidating the impact of disease-causing mutations will be to map sites of RNA-protein interactions occurring in the context of living cells. These comprehensive maps will be leveraged to identify disease-causing mutations with the potential to abolish or create protein-binding sites within RNA transcripts. Our computational predictions of toxic RNA elements will be validated in the laboratory using patient-derived cell lines to assay RNA processing of the endogenous disease-gene. Our work in this area promises to improve our understanding of the basic mechanisms governing gene expression and will directly translate to improved diagnosis and treatment of aging related diseases. [More]

Bill Saxton, Dept. MCD Biology

The Saxton lab studies mechanisms that drive intracellular transport and cytoplasmic organization, using Drosophila as a model organism. To generate and maintain proper cytoplasmic order and thus their complex functions, cells use microtubules and force-generating motor proteins to transport RNAs, proteins, mitochondria and other organelles to appropriate locations. Neurons are especially dependent on such microtubule-based cytoplasmic transport, because their signaling functions rely on extraordinarily long cytoplasmic extensions (axons and dendrites) that require import of many components from their cell bodies ... [More]

Don Smith, Microbiology and Environmental Toxicology

It is becoming clear that exposures to environmental toxins, such as lead, mercury, and arsenic can cause or contribute to the development of diseases in humans. For example, some neurobehavioral and neurodegenerative disorders, such as learning deficits and Parkinsonism have been linked to elevated lead and manganese exposures in children and manganese exposures in adults, respectively. The Smith lab explores basic mechanisms underlying how toxic metal exposures contributes to cellular effects and disease. [More]

Michael Stone, Dept. of Chemistry and Biochemistry

The Stone Research Group combines the use of biochemical and structural methods with newly emerging single-molecule techniques to probe the dynamics of protein-nucleic acid interactions and the molecular mechanisms of biological motors.  Our current area of focus is the structure and function of the telomerase ribonucleoprotein, an RNA-dependent DNA polymerase that maintains genomic stability by synthesizing repetitive DNA sequences at chromosome termini.  These short DNA repeats provide the foundation for specialized chromatin structures, called telomeres, which prevent deleterious chromosome fusion events by differentiating chromosome ends from sites of DNA damage.  It has been shown that telomere length typically decreases with every round of cell division, leading to the so-called ‘molecular clock’ hypothesis, wherein telomere length serves as a signal to control cellular lifespan. This notion is consistent with the finding that active telomere DNA synthesis is normally restricted to rapidly dividing cell types such as stem cells and the majority of human cancers. Our research seeks to elucidate physical mechanisms governing telomere length regulation, and in turn establish a conceptual framework within which to develop novel diagnostic and therapeutic strategies for human disease. [More]

Yi Zuo, Dept. of MCD Biology