期刊
JOURNAL OF CELL SCIENCE
卷 128, 期 12, 页码 2363-2373出版社
COMPANY BIOLOGISTS LTD
DOI: 10.1242/jcs.169466
关键词
Acidocalcisome; Calcium; Contractile vacuole; Polyphosphate; Vacuolar pyrophosphatase
类别
资金
- US National Institutes of Health (NIH) [AI107663]
- NIH [AI101167]
- Conselho Nacional de Desenvolvimento Cientifico e Tecnologico (CNPq-Universal grants, INCT em Biologia Estrutural e Bioimagem) [480184/2012-7, 449256/2014-6]
- Fundacao Carlos Chagas Filho de Amparo a Pesquisa do Estado do Rio de Janeiro (FAPERJ-Programa Nucleos Emergentes grant) [E-26/111.185/2011]
- Coordenacao de Aperfeicoamento do Pessoal de Nivel Superior (CAPES)
- Financiadora de Estudos e Projetos (FINEP)
The contractile vacuole complex (CVC) of Trypanosoma cruzi, the etiologic agent of Chagas disease, collects and expels excess water as a mechanism of regulatory volume decrease after hyposmotic stress; it also has a role in cell shrinking after hyperosmotic stress. Here, we report that, in addition to its role in osmoregulation, the CVC of T. cruzi has a role in the biogenesis of acidocalcisomes. Expression of dominant-negative mutants of the CVC-located small GTPase Rab32 (TcCLB.506289.80) results in lower numbers of less-electron-dense acidocalcisomes, lower content of polyphosphate, lower capacity for acidocalcisome acidification and Ca2+ uptake that is driven by the vacuolar proton pyrophosphatase and the Ca2+-ATPase, respectively, as well as less-infective parasites, revealing the role of this organelle in parasite infectivity. By using fluorescence, electron microscopy and electron tomography analyses, we provide further evidence of the active contact of acidocalcisomes with the CVC, indicating an active exchange of proteins between the two organelles.
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