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TGF-Betas May Be Involved In Determining Timing Of Vulnerability To Cell Death

 
  October, 19 2000 0:55
your information resource in human molecular genetics
 
     
Death takes a holiday

The transforming growth factor beta (TGF-beta) proteins are jacks of all trades during development, participating in a wide range of functions. However, they were not thought to be involved in brain growth, as knocking out the gene for TGF-beta 1, 2 or 3 alone produces no effect on neurons. Surprisingly, though, Kerstin Krieglstein and colleagues show in the November 2000 issue of Nature Neuroscience (Vol. 3, No. 11, pp. 1085-1090), that simultaneously blocking the function of all three TGF-beta proteins in the chick embryo almost completely prevents programmed cell death in many areas of the nervous system. Neuron number in the developing brain is normally controlled by a two-step process. Many more neurons are born than needed, and then a large fraction of them die by apoptosis during a restricted period of early life. How many neurons survive is thought to be controlled by competition for a limited supply of growth factors supplied by their target tissues. When Krieglstein and colleagues used a neutralizing antibody or a protein fragment derived from the TGF-beta receptor to block TGF-beta function, they found that these treatments prevented cell death as effectively as blocking caspase-3, a key step in the execution phase of apoptosis, even when the target tissue (the limb bud) was removed completely. Interestingly, however, adding extra TFG-beta to normal animals does not increase cell death, suggesting that these proteins do not kill neurons outright, but may instead create a 'permissive environment' for programmed cell death. This raises the possibility that TGF-betas may be involved in determining the timing of vulnerability to cell death during development, which is supported by evidence that their expression increases precisely during this vulnerable period.

Richard Miller and Clifton Ragsdale discuss the work in an accompanying News & Views article (pp. 1061-1062).

Contacts:

Dr. Kerstin Krieglstein
Department of Anatomy
University of Saarland
Building 61
D-66421 Homburg
Germany
tel: +49 6841 16 6103
fax: +49 6841 16 6104
e-mail: ankkri@med-rz.uni-sb.de

Dr. Richard J. Miller
Dept of Neurobiology, Pharmacology, and Physiology
University of Chicago
947 E. 58th Street
Chicago, Illinois 60637
USA
tel: +1 773 702 9336
fax: +1 773 702 5903
e-mail: rjmx@midway.uchicago.edu

(C) Nature Neuroscience press release.


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