Violacein-Induced Chaperone System Collapse Underlies Multistage Antiplasmodial Activity.
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Tavella Tatyana Almeida, da Silva Noeli Soares Melo, Spillman Natalie, Kayano Ana Carolina Andrade Vitor, Cassiano Gustavo Capatti, Vasconcelos Adrielle Ayumi, Camargo Antônio Pedro, da Silva Djane Clarys Baia, Fontinha Diana, Salazar Alvarez Luis Carlos, Ferreira Letícia Tiburcio, Peralis Tomaz Kaira Cristina, Neves Bruno Junior, Almeida Ludimila Dias, Bargieri Daniel Youssef, Lacerda Marcus Vinicius Guimarães de, Lemos Cravo Pedro Vitor, Sunnerhagen Per, Prudêncio Miguel, Andrade Carolina Horta, Pinto Lopes Stefanie Costa, Carazzolle Marcelo Falsarella, Tilley Leann, Bilsland Elizabeth, Borges Júlio César, Maranhão-Costa Fabio Trindade
Аннотация
Antimalarial drugs with novel modes of action and wide therapeutic potential are needed to pave the way for malaria eradication. Violacein is a natural compound known for its biological activity against cancer cells and several pathogens, including the malaria parasite, Plasmodium falciparum (Pf). Herein, using chemical genomic profiling (CGP), we found that violacein affects protein homeostasis. Mechanistically, violacein binds Pf chaperones, PfHsp90 and PfHsp70-1, compromising the latter's ATPase and chaperone activities. Additionally, violacein-treated parasites exhibited increased protein unfolding and proteasomal degradation. The uncoupling of the parasite stress response reflects the multistage growth inhibitory effect promoted by violacein. Despite evidence of proteotoxic stress, violacein did not inhibit global protein synthesis via UPR activation-a process that is highly dependent on chaperones, in agreement with the notion of a violacein-induced proteostasis collapse. Our data highlight the importance of a functioning chaperone-proteasome system for parasite development and differentiation. Thus, a violacein-like small molecule might provide a good scaffold for development of a novel probe for examining the molecular chaperone network and/or antiplasmodial drug design.