Control of erythroid cell production via caspase-mediated cleavage of transcription factor SCL/Tal-1 View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2003-08

AUTHORS

A Zeuner, A Eramo, U Testa, N Felli, E Pelosi, G Mariani, S M Srinivasula, E S Alnemri, G Condorelli, C Peschle, R De Maria

ABSTRACT

SCL/Tal-1 is a helix-loop-helix (HLH) transcription factor required for blood cell development, whose abnormal expression is responsible for induction of T-cell acute lymphoblastic leukemia. We show here that SCL/Tal-1 is a key target of caspases in developing erythroblasts. SCL/Tal-1 degradation occurred rapidly after caspase activation and preceded the cleavage of the major erythroid transcription factor GATA-1. Expression of a caspase-resistant SCL/Tal-1 in erythroid progenitors was able to prevent amplification of caspase activation, GATA-1 degradation and impaired erythropoiesis induced by growth factor deprivation or death receptor triggering. The potent proerythropoietic activity of uncleavable SCL/Tal-1 was clearly evident in the absence of erythropoietin, a condition that did not allow survival of normal erythroid cells or expansion of erythroblasts expressing caspase-resistant GATA-1. In the absence of erythropoietin, cells expressing caspase-resistant SCL/Tal-1 maintain high levels of Bcl-X(L), which inhibits amplification of the caspase cascade and mediates protection from apoptosis. Thus, SCL/TAL-1 is a survival factor for erythroid cells, whereas caspase-mediated cleavage of SCL/Tal-1 results in amplification of caspase activation, GATA-1 degradation and impaired erythropoiesis. More... »

PAGES

4401255

Identifiers

URI

http://scigraph.springernature.com/pub.10.1038/sj.cdd.4401255

DOI

http://dx.doi.org/10.1038/sj.cdd.4401255

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1000777530

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/12867998


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