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Dr Erik Griffin

Associate Professor

Email:  

Phone: 024 765 28976

Office: B121


Research Clusters

Cells & Development


Opportunities in the group

For PhD and postdoctoral opportunities, and interest in potential collaborations, please contact me at the above email address.

Research/Teaching Interests

All animals begin life as a single cell, the newly fertilized egg. As embryos develop, they generate the diverse array of cell types that make up the adult organism. We are interested in understanding how embryos generate diverse cell types, with a focus on the process of asymmetric cell division. When a cell divides asymmetrically, it generates two daughter cells with different functions, fates or sizes. For example, stem cells often divide asymmetrically to generate a stem cell and a cell that differentiates.

We use the embryo of the nematode worm C. elegans to study the mechanisms of asymmetric cell division. Shortly after fertilization, the one-cell cell C. elegans embryo divides asymmetrically to give rise to a somatic and a germline daughter cell. This process is controlled by a conserved group of cell polarity regulators called the PAR proteins. The PAR proteins orchestrate the partitioning of cytoplasmic RNA-binding proteins to either the somatic or germline daughter cell. These RNA-binding proteins establish the distinct translation programs that give these cells their unique identities. We are interested in two key questions. First, how do the PAR proteins, which concentrate the cell cortex/plasma membrane control the segregation of RNA-binding proteins deep in the cytoplasm? Second, how do these RNA-binding proteins function to either activate or repress the translation of target mRNAs? We approach these questions by combining quantitative live imaging with genetic and biochemical approaches.

Research: Technical Summary

Coordinating cell polarity and the cell cycle

Coordination between the cell polarity and cell cycle mechanisms ensure that factors are localized to the right place at the right time during asymmetric cell division. Interestingly, we recently found that the cell cycle kinase PKL-1 (Polo-like kinase) controls the segregation of germplasm factors during the asymmetric division of the one-cell C. elegans embryo. PLK-1 concentrates the anterior cytoplasmic domain where it inhibits the accumulation of at least two germplasm proteins, POS-1 and MEX-1. As a result, POS-1 and MEX-1 segregate to the posterior, germline daughter cell where they regulate the translation of important patterning genes. We are currently asking whether PLK-1 also drives the polarization of other germplasm factors. Additionally, we are interested in characterizing the phosphatases they may counteract PLK-1 kinase to support germplasm segregation.

How asymmetric division regulates translation

As in most animal embryos, the patterning of the early C. elegans embryo reflects the regulated translation of maternal mRNAs at specific stages and in specific cells. These translational patterns derive, at least in part, from the segregation of RNA-binding proteins during asymmetric cell division. We are interested in developing and using quantitative live-imaging approaches to dissect how translation is controlled in space and time in the early embryo.

  • 2024 - present, Associate Professor, SLS, University of Warwick
  • 2019 – 2023, Associate Professor, Department of Biology, Dartmouth College, Hanover NH
  • 2012 – 2019, Assistant Professor, Department of Biology, Dartmouth College, Hanover NH
  • 2006 – 2012, Postdoctoral Scholar, Johns Hopkins University School of Medicine
  • 2000 - 2006 PhD, California Institute of Technology, Pasadena CA