Malaria parasites do respond to heat. Issue 6 (June 2022)

• Record Type: Journal Article
• Authors: Tintó-Font, Elisabet; Cortés, Alfred
• Is Part Of: Trends in parasitology. Volume 38:Issue 6(2022)
• Page Start: 435
• Page End: 449
• Publication Date: 2022-06
• Subjects: Plasmodium falciparum -- adaptation -- directed transcriptional response -- heat shock response -- fever -- PfAP2-HS; Parasitology -- Periodicals; Parasitology -- Periodicals; Biology -- Periodicals; Parasitology; Biology; Parasitologie -- Périodiques; Online resources; 571.999
• DOI: 10.1016/j.pt.2022.02.009
• Languages: English
• ISSNs: 1471-4922

Abstract

Abstract : The capacity of malaria parasites to respond to changes in their environment at the transcriptional level has been the subject of debate, but recent evidence has unambiguously demonstrated that Plasmodium spp. can produce adaptive transcriptional responses when exposed to some specific types of stress. These include metabolic conditions and febrile temperature. The Plasmodium falciparum protective response to thermal stress is similar to the response in other organisms, but it is regulated by a transcription factor evolutionarily unrelated to the conserved transcription factor that drives the heat shock (HS) response in most eukaryotes. Of the many genes that change expression during HS, only a subset constitutes an authentic response that contributes to parasite survival. Highlights: It is often difficult to distinguish which changes in gene expression upon stress constitute an authentic protective response and which ones simply reflect cell damage or death. Recent research has demonstrated that malaria parasites can produce directed responses to some changes in their environment at the transcriptional level. These include protective responses to specific metabolic conditions and to heat stress. Unlike the majority of eukaryotes, in which the canonical heat shock (HS) response is orchestrated by the conserved HSF1 transcription factor, the Plasmodium falciparum canonical HS response is driven by PfAP2-HS, an ApiAP2 transcription factor. The PfAP2-HS-driven HS response is analogous to the universally conserved protective HS response, as it involves a rapid and transient increase in the expression of a small number of chaperone-encoding genes.