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C. elegans embryonic development
Asymmetric cell division, which produces two daughter cells with different properties and different
developmental potentials, is one of the most fundamental mechanisms in development used to generate a diverse array of cell
types. In order to achieve asymmetric division, a cell must polarize cytoskeleton and unequally segregate cellular contents
(e.g. proteins and RNAs). But how is this actually done? How does a cell know, for example, the orientation to which the
cytoskeleton should be polarized? We are interested in understanding the mechanism of asymmetric division and how it is
regulated with respect to other events in development using C. elegans as a model system.
In C. eleganss, embryonic germ cells, which eventually give rise to a whole animal, possess a remarkable ability
to maintain the totipotency, or the potential to become differentiated into any cell types. Importantly, this potential is
restricted to only one of the daughters at each cell division; that is, the division of a germ cell is asymmetric. We now know
that a germ cell-specific nuclear protein called PIE-1 acts as an ON/OFF switch between the differentiated state (ON) and the
undifferentiated stem cell state (OFF). If PIE-1 is missing (due to a mutation in the pie-1 gene), both daughters of a
germ cell become committed to differentiation, indicating that PIE-1 functions as a differentiation inhibitor. Moreover,
PIE-1 is inherited by only one of the daughters at each division, and the cell that receives PIE-1 inevitably becomes a new
germ cell. One of our goals is to uncover molecular mechanisms responsible for asymmetric localization of PIE-1 and mechanisms
by which PIE-1 mediates differentiation inhibition. C. elegans provides an excellent opportunity to study development
as it offers a battery of genetics tools as well as molecular and biochemical techniques. Through the analysis of PIE-1 and
other developmentally important factors, we are hoping to get one step closer to the big mystery of biology; i.e. how each of
the molecular events including asymmetric division, signal transduction and transcriptional/translational regulation is
coordinated such that a single cell, the fertilized egg, can ultimately give rise to a complex organism.
Selected Publications
Bobola N, Jansen RP, Shin TH, Nasmyth K (1996) Asymmetric accumulation of Ash1p in
postanaphase nuclei depends on a myosin and restricts yeast mating-type switching to mother cells. Cell
84:699-709.
Zachariae W*, Shin TH*, Galova M, Obermaier B, Nasmyth K (1996) Identification of subunits of the
anaphase-promoting complex of Saccharomyces cerevisiae. Science 274:1201-1204. (*Equal contribution)
Batchelder C, Dunn MA, Choy B, Suh Y, Cassie C, Shim EY, Shin TH, Mello CC, Seydoux G, Blackwell TK (1999)
Transcriptional repression by the Caenorhabditis elegans germ-line protein PIE-1. Genes and Development
13:202-212.
Rocheleau CE*, Yasuda J*, Shin TH*, Lin R, Sawa H, Okano H, Priess JR, Davis RJ, Mello CC (1999) WRM-1
activates the LIT-1 protein kinase to transduce anterior/posterior polarity signals in C. elegans. Cell
97:717-726. (*Equal contribution)
Shin TH*, Yasuda J*, Rocheleau CE*, Lin R, Soto M, Bei Y, Davis RJ, Mello CC (1999) MOM-4, a MAP kinase
kinase kinase-related protein, activates WRM-1/LIT-1 kinase to transduce anterior/posterior polarity signals in
C. elegans. Molecular Cell 4:275-280. (*Equal contribution)
Unhavaithaya Y*, Shin TH*, Miliaras N, Lee J, Oyama T, Mello CC (2002) MEP-1 and a homolog of the NURD
complex component Mi-2 act together to maintain germline-soma distinctions in C. elegans. Cell
111:991-1002. (*Equal contribution)
Shin TH, Mello CC (2003) Chromatin regulation during C. elegans germline development. Current
Opinion in Genetics and Development 13:455-462.
Contact Information
- Tae Ho Shin, Ph.D.
- Department of Molecular and Cellular Biology
- Baylor College of Medicine
- One Baylor Plaza N604A
- Houston, Texas 77030, U.S.A.
- Tel: (713) 798-4683
- Fax: (713) 798-3617
- E-mail: tshin@bcm.tmc.edu
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