Molecular analysis of heterochronic gene lin-14 and developmental cell cycle control in Caenorhabditis elegans.

1999 ◽  
Author(s):  
Yang Hong
2006 ◽  
Vol 48 (1) ◽  
pp. 25-32 ◽  
Author(s):  
Tadao Inoue ◽  
Kazumasa Hirata ◽  
Yuichiro Kuwana ◽  
Masahiro Fujita ◽  
Johji Miwa ◽  
...  

2007 ◽  
Vol 292 (1) ◽  
pp. C269-C277 ◽  
Author(s):  
Xiaoyan Yin ◽  
Jerod Denton ◽  
Xiaohui Yan ◽  
Kevin Strange

An inwardly rectifying swelling- and meiotic cell cycle-regulated anion current carried by the ClC channel splice variant CLH-3b dominates the whole cell conductance of the Caenorhabditis elegans oocyte. Oocytes also express a novel outwardly rectifying anion current termed ICl,OR. We recently identified a worm strain carrying a null allele of the clh-3 gene and utilized oocytes from these animals to characterize ICl,OR biophysical properties. The ICl,OR channel is strongly voltage dependent. Outward rectification is due to voltage-dependent current activation at depolarized voltages and rapid inactivation at voltages more hyperpolarized than approximately +20 mV. Apparent channel open probability is zero at voltages less than +20 mV. The channel has a 4:1 selectivity for Cl− over Na+ and an anion selectivity sequence of SCN− > I− > Br− > Cl− > F−. ICl,OR is relatively insensitive to most conventional anion channel inhibitors including DIDS, 4,4′-dinitrostilbene-2,2′-disulfonic acid, 9-anthracenecarboxylic acid, and 5-nitro-2-(3-phenylpropylamino)benzoic acid. However, the current is rapidly inhibited by niflumic acid, metal cations including Gd3+, Cd2+, and Zn2+, and bath acidification. The combined biophysical properties of ICl,OR are distinct from those of other anion currents that have been described. During oocyte meiotic maturation, ICl,OR activity is rapidly downregulated, suggesting that the channel may play a role in oocyte Cl− homeostasis, development, cell cycle control, and/or ovulation.


Oncogene ◽  
2005 ◽  
Vol 24 (17) ◽  
pp. 2756-2764 ◽  
Author(s):  
John Koreth ◽  
Sander van den Heuvel

2010 ◽  
Vol 21 (5) ◽  
pp. 725-738 ◽  
Author(s):  
Alexandra Segref ◽  
Juan Cabello ◽  
Caroline Clucas ◽  
Ralf Schnabel ◽  
Iain L. Johnstone

Coordination between cell fate specification and cell cycle control in multicellular organisms is essential to regulate cell numbers in tissues and organs during development, and its failure may lead to oncogenesis. In mammalian cells, as part of a general cell cycle checkpoint mechanism, the F-box protein β-transducin repeat-containing protein (β-TrCP) and the Skp1/Cul1/F-box complex control the periodic cell cycle fluctuations in abundance of the CDC25A and B phosphatases. Here, we find that the Caenorhabditis elegans β-TrCP orthologue LIN-23 regulates a progressive decline of CDC-25.1 abundance over several embryonic cell cycles and specifies cell number of one tissue, the embryonic intestine. The negative regulation of CDC-25.1 abundance by LIN-23 may be developmentally controlled because CDC-25.1 accumulates over time within the developing germline, where LIN-23 is also present. Concurrent with the destabilization of CDC-25.1, LIN-23 displays a spatially dynamic behavior in the embryo, periodically entering a nuclear compartment where CDC-25.1 is abundant.


2001 ◽  
Vol 120 (5) ◽  
pp. A322-A322
Author(s):  
M STALLS ◽  
J SUN ◽  
K THOMPSON ◽  
N VANHOUTEN

2006 ◽  
Vol 175 (4S) ◽  
pp. 317-317
Author(s):  
Xifeng Wu ◽  
Jian Gu ◽  
H. Barton Grossman ◽  
Christopher I. Amos ◽  
Carol Etzel ◽  
...  

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