scholarly journals The FoxF/FoxC factor LET-381 directly regulates both cell fate specification and cell differentiation in C. elegans mesoderm development

Development ◽  
2010 ◽  
Vol 137 (9) ◽  
pp. 1451-1460 ◽  
Author(s):  
N. M. Amin ◽  
H. Shi ◽  
J. Liu
Keyword(s):  
Cell Differentiation ◽  
Cell Fate ◽  
Cell Fate Specification ◽  
Mesoderm Development ◽  
Fate Specification ◽  
C Elegans

Genes necessary for C. elegans cell and growth cone migrations

Development ◽  
1997 ◽  
Vol 124 (9) ◽  
pp. 1831-1843 ◽  
Author(s):  
W.C. Forrester ◽  
G. Garriga
Keyword(s):  
Cell Fate ◽  
Single Gene ◽  
Growth Cones ◽  
Cell Fate Specification ◽  
Fate Specification ◽  
C Elegans ◽  
Final Destination ◽  
Multiple Cell

The migrations of cells and growth cones contribute to form and pattern during metazoan development. To study the mechanisms that regulate cell motility, we have screened for C. elegans mutants defective in the posteriorly directed migrations of the canal-associated neurons (CANs). Here we describe 14 genes necessary for CAN cell migration. Our characterization of the mutants has led to three conclusions. First, the mutations define three gene classes: genes necessary for cell fate specification, genes necessary for multiple cell migrations and a single gene necessary for final positioning of migrating cells. Second, cell interactions between the CAN and HSN, a neuron that migrates anteriorly to a position adjacent to the CAN, control the final destination of the HSN cell body. Third, C. elegans larval development requires the CANs. In the absence of CAN function, larvae arrest development, with excess fluid accumulating in their pseudocoeloms. This phenotype may reflect a role of the CANs in osmoregulation.

scholarly journals Transcriptional upregulation of the C. elegans Hox gene lin-39 during vulval cell fate specification

2006 ◽  
Vol 123 (2) ◽  
pp. 135-150 ◽  
Author(s):  
Javier A. Wagmaister ◽  
Julie E. Gleason ◽  
David M. Eisenmann
Keyword(s):  
Cell Fate ◽  
Cell Fate Specification ◽  
Hox Gene ◽  
Fate Specification ◽  
C Elegans

scholarly journals Mab21, the mouse homolog of a C. elegans cell-fate specification gene, participates in cerebellar, midbrain and eye development

1998 ◽  
Vol 79 (1-2) ◽  
pp. 131-135 ◽  
Author(s):  
M. Mariani ◽  
A. Corradi ◽  
D. Baldessari ◽  
N. Malgaretti ◽  
O. Pozzoli ◽  
...  
Keyword(s):  
Cell Fate ◽  
Eye Development ◽  
Cell Fate Specification ◽  
Mouse Homolog ◽  
Fate Specification ◽  
C Elegans

An essential role for the Drosophila Pax2 homolog in the differentiation of adult sensory organs

Development ◽  
1999 ◽  
Vol 126 (10) ◽  
pp. 2261-2272 ◽  
Author(s):  
J. Kavaler ◽  
W. Fu ◽  
H. Duan ◽  
M. Noll ◽  
J.W. Posakony
Keyword(s):  
Cell Differentiation ◽  
Cell Fate ◽  
Essential Role ◽  
Mitotic Cell ◽  
The Body ◽  
Cell Fate Specification ◽  
Loss Of Function ◽  
Fate Specification ◽  
High Level ◽  
Pax2 Expression

The adult peripheral nervous system of Drosophila includes a complex array of mechanosensory organs (bristles) that cover much of the body surface of the fly. The four cells (shaft, socket, sheath, and neuron) which compose each of these organs adopt distinct fates as a result of cell-cell signaling via the Notch (N) pathway. However, the specific mechanisms by which these cells execute their conferred fates are not well understood. Here we show that D-Pax2, the Drosophila homolog of the vertebrate Pax2 gene, has an essential role in the differentiation of the shaft cell. In flies bearing strong loss-of-function mutations in the shaven function of D-Pax2, shaft structures specifically fail to develop. Consistent with this, we find that D-Pax2 protein is expressed in all cells of the bristle lineage during the mitotic (cell fate specification) phase of bristle development, but becomes sharply restricted to the shaft and sheath cells in the post-mitotic (differentiative) phase. Two lines of evidence described here indicate that D-Pax2 expression and function is at least in part downstream of cell fate specification mechanisms such as N signaling. First, we find that the lack of late D-Pax2 expression in the socket cell (the sister of the shaft cell) is controlled by N pathway activity; second, we find that loss of D-Pax2 function is epistatic to the socket-to-shaft cell fate transformation caused by reduced N signaling. Finally, we show that misexpression of D-Pax2 is sufficient to induce the production of ectopic shaft structures. From these results, we propose that D-Pax2 is a high-level transcriptional regulator of the shaft cell differentiation program, and acts downstream of the N signaling pathway as a specific link between cell fate determination and cell differentiation in the bristle lineage.

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