Cell fate determination in the peripheral nervous system: The sympathoadrenal progenitor

1993 ◽  
Vol 24 (2) ◽  
pp. 185-198 ◽  
Author(s):  
David J. Anderson
Keyword(s):  
Nervous System ◽  
Peripheral Nervous System ◽  
Cell Fate ◽  
Cell Fate Determination ◽  
Fate Determination

A critical role for Cyclin E in cell fate determination in the central nervous system of Drosophila melanogaster

2004 ◽  
Vol 7 (1) ◽  
pp. 56-62 ◽  
Author(s):  
Christian Berger ◽  
S. K. Pallavi ◽  
Mohit Prasad ◽  
L. S. Shashidhara ◽  
Gerhard M. Technau
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Drosophila Melanogaster ◽  
Cell Fate ◽  
Cyclin E ◽  
Critical Role ◽  
Cell Fate Determination ◽  
Fate Determination ◽  
The Central Nervous System

Cell fate determination in an annelid equivalence group

Development ◽  
1996 ◽  
Vol 122 (6) ◽  
pp. 1839-1847 ◽  
Author(s):  
F.Z. Huang ◽  
D.A. Weisblat
Keyword(s):  
Nervous System ◽  
Cell Fate ◽  
Cell Fate Determination ◽  
Equivalence Group ◽  
Group Interactions ◽  
Fate Determination ◽  
Blast Cells ◽  
Transient Contact ◽  
Necessary And Sufficient

In embryos of glossiphoniid leeches such as Helobdella triserialis and H. robusta, pairs of adjacent ‘o/p’ ectodermal blast cells are known to be developmentally equipotent and yet eventually contribute distinct sets of ‘O’ and ‘P’ progeny to the nervous system and epidermis of the mature leech. It has been thought that the fate-determining interactions in this ‘O-P equivalence group’ take place between the equipotent cells themselves. We show here that such intra-group interactions are neither necessary nor sufficient. Instead, transient contact with cells in another ectodermal lineage is necessary and sufficient to induce o/p blast cells to assume the P fate. In the absence of this contact they assume the O fate.

The Drosophila sanpodo gene controls sibling cell fate and encodes a tropomodulin homolog, an actin/tropomyosin-associated protein

Development ◽  
1998 ◽  
Vol 125 (10) ◽  
pp. 1845-1856 ◽  
Author(s):  
C.A. Dye ◽  
J.K. Lee ◽  
R.C. Atkinson ◽  
R. Brewster ◽  
P.L. Han ◽  
...  
Keyword(s):  
Nervous System ◽  
Embryonic Development ◽  
Notch Signaling ◽  
Peripheral Nervous System ◽  
Cell Fate ◽  
Genetic Interaction ◽  
Cell Fate Determination ◽  
Loss Of Function ◽  
Protein Loss ◽  
Sensory Structures

Notch signaling is required in many invertebrate and vertebrate cells to promote proper cell fate determination. Mutations in sanpodo cause many different neuronal peripheral nervous system precursor cells to generate two identical daughter neurons, instead of a neuron and sibling cell. This phenotype is similar to that observed when Notch function is lost late in embryonic development and opposite to the numb loss-of-function phenotype. Genetic interaction studies show that sanpodo is epistatic to numb. sanpodo encodes a homolog of tropomodulin, an actin/tropomyosin-associated protein. Loss of sanpodo leads to an aberrant F-actin distribution and causes differentiation defects of actin-containing sensory structures. Our data suggest that an actin-based process is involved in Notch signaling.

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