Biology

My overarching goal is to understand how cell growth triggers cell division. Linking growth to division is important because it allows cells to maintain a specific size range to best perform their physiological functions. For example, red blood cells must be small enough to flow through small capillaries, whereas macrophages must be large enough to engulf pathogens. In addition to being important for normal cell and tissue physiology, the link between growth and division is misregulated in cancer.

I study how ecological communities assemble and influence ecosystem processes, focusing on the role of microbial symbioses, which are ubiquitous in plants and animals. My research is driven primarily by intellectual curiosity about the unseen organisms that shape our planet, but is also aimed to provide knowledge that can be used to better manage ecosystem responses to global change, agriculture, and human health.

Our lab study neural circuits underlying motivated behaviors and how maladaptive change in these circuits causing neuropsychiatric disorders. We currently focuse on pain and addiction. Both conditions trigger highly motivated behaviors, and the transition to chronic pain and to compulsive drug use involves maladaptive changes of the underlying neuronal circuitry. 

Neuroal circuits mediating opioid addiction:

The overall goal of my research program is to understand how stem cell-like populations are created and maintained in the context of an intact and environmental responsive tissue.  We use the Arabidopsis stomatal lineage for these studies as this epidermal cell lineage distills many of the features common to all tissue development: stomatal precursor cells are chosen from an initially equivalent field, they undergo asymmetric and self-renewing divisions, they communicate among themselves to establish pattern and they terminally differentiate into stable, physiologically important cell-types

The regulation of chromatin structure is essential for all eukaryotic organisms. Our research interests are to determine the contribution of chromatin to mechanisms that maintain genomic integrity and metabolic homeostasis in the context of disease and development. We utilize a varied experimental approach that includes computational, biochemical, molecular and cellular assays in both yeast and mammalian systems to ascertain the contribution of chromatin remodelers and histone modifiers to carcinogen susceptibility and metabolic gene expression.

By studying calcineurin, the conserved Ca2+/calmodulin-regulated protein phosphatase, we aim to discover and elucidate new Ca2+-regulated signaling pathways in humans. The calcineurin phosphatase dephosphorylates proteins only when Ca2+ signaling is triggered, for example by a hormone, growth factor, neurotransmitter etc. Previous work from the Cyert lab discovered how calcineurin allows yeast cells to survive environmental stress (Goldman et al, 2014, Molecular Cell).

The Kopito laboratory seeks a molecular understanding of how cells maintain the fidelity of their proteomes. Unlike DNA, which can be repaired if damaged or incorrectly made, proteins cannot be mended. Instead, damaged or incorrectly synthesized proteins must be rapidly and efficiently destroyed lest they form toxic aggregates.