期刊
BIOCHEMICAL SOCIETY TRANSACTIONS
卷 41, 期 -, 页码 934-938出版社
PORTLAND PRESS LTD
DOI: 10.1042/BST20130052
关键词
differentiation; quiescence; rapamycin; target of rapamycin complex 4 (TORC4); trypanosome
资金
- Miguel Servet fellowship [CP09/00300]
- Spanish Ministerio de Ciencia e Innovacion, Plan Nacional [SAF2012-40029]
- Junta de Andalucia [CTS-5841]
- Red de Investigacion Cooperativa en Enfermedades Tropicales (RICET) [RD06/0001/0010]
The complex life cycle of Trypanosoma brucei provides an excellent model system to understand signalling pathways that regulate development. We described previously the classical functions of TOR (target of rapamycin) 1 and TOR2 in T. brucei. In a more recent study, we described a novel TOR kinase, named TOR4, which regulates differentiation from the proliferative infective form to the quiescent form. In contrast with TOR1 loss-of-function, down-regulation of TOR4 triggers an irreversible differentiation process through the development of the insect pre-adapted quiescent form. TOR4 governs a signalling pathway distinct from those controlled by the conventional TOR complexes TORC1 and TORC2. Depletion of TOR4 induces all well-known characteristics of the quiescent developmental stage in trypanosomes, including expression of the PAD (proteins associated with differentiation) surface proteins and transcriptional down-regulation of the VSG (variant surface glycoprotein) gene. TOR4 kinase forms a structurally and functionally distinct complex named TORC4. TOR4 associates with LST8 (lethal with sec-13 protein 8) and other factors including an armadillo-domain-containing protein and the major vault protein, which probably serves as a scaffold for this kinase. Research in T. brucei, a protozoan parasite that diverged from the eukaryotic tree early in evolution, may help to uncover new functions of TOR kinases.
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