Rac1/WAVE2 and Cdc42/N-WASP Participation in Actin-Dependent Host Cell Invasion by Extracellular Amastigotes of Trypanosoma cruzi

Autor(es)

Bonfim-Melo, Alexis ^[1] ; Ferreira, Eden R. ^[1] ; Mortara, Renato A. ^[1]

Afiliação do(s) autor(es)

^[1] Univ Fed Sao Paulo, Escola Paulista Med, Dept Microbiol Imunol & Parasitol, Sao Paulo - Brazil

• Tipo de documento: Artigo Científico
• Fonte: FRONTIERS IN MICROBIOLOGY; v. 9, FEB 28 2018.
• Citações Web of Science: 7

Resumo

This study evaluated the participation of host cell Rho-family GTPases and their effector proteins in the actin-dependent invasion by Trypanosoma cruzi extracellular amastigotes (EAs). We observed that all proteins were recruited and colocalized with actin at EA invasion sites in live or fixed cells. EA internalization was inhibited in cells depleted in Rac1, N-WASP, and WAVE2. Time-lapse experiments with Rac1, N-WASP and WAVE2 depleted cells revealed that EA internalization kinetics is delayed even though no differences were observed in the proportion of EA-induced actin recruitment in these groups. Overexpression of constitutively active constructs of Rac1 and RhoA altered the morphology of actin recruitments to EA invasion sites. Additionally, EA internalization was increased in cells overexpressing CA-Rac1 but inhibited in cells overexpressing CA-RhoA. WT-Cdc42 expression increased EA internalization, but curiously, CA-Cdc42 inhibited it. Altogether, these results corroborate the hypothesis of EA internalization in non-phagocytic cells by a phagocytosis-like mechanism and present Rac1 as the key Rho-family GTPase in this process. (AU)

• Processo FAPESP: 11/51475-3 - Biologia molecular e celular do parasitismo por Trypanosoma cruzi
• Beneficiário: José Franco da Silveira Filho
• Modalidade de apoio: Auxílio à Pesquisa - Temático
• Processo FAPESP: 12/21335-8 - As vias de Cdc42/N-WASP e Rac1/WAVE2 na dinâmica de actina durante a invasão celular pelos amastigotas extracelulares de Trypanosoma cruzi
• Beneficiário: Alexis de Sá Ribeiro do Bonfim de Melo
• Modalidade de apoio: Bolsas no Brasil - Doutorado