Paternal effect of the nuclear formin-like protein MISFIT on Plasmodium development in the mosquito vector.

Malaria parasites must undergo sexual and sporogonic development in mosquitoes before they can infect their vertebrate hosts. We report the discovery and characterization of MISFIT, the first protein with paternal effect on the development of the rodent malaria parasite Plasmodium berghei in Anophel...

Descripción completa

Guardado en:

Detalles Bibliográficos
Autores principales:	Ellen S C Bushell, Andrea Ecker, Timm Schlegelmilch, David Goulding, Gordon Dougan, Robert E Sinden, George K Christophides, Fotis C Kafatos, Dina Vlachou
Formato:	article
Lenguaje:	EN
Publicado:	Public Library of Science (PLoS) 2009
Materias:	Immunologic diseases. Allergy RC581-607 Biology (General) QH301-705.5
Acceso en línea:	https://doaj.org/article/2f831be0a4194a9ea3b394ac3dedb1f0
Etiquetas:	Agregar Etiqueta Sin Etiquetas, Sea el primero en etiquetar este registro!

id	oai:doaj.org-article:2f831be0a4194a9ea3b394ac3dedb1f0
record_format	dspace
spelling	oai:doaj.org-article:2f831be0a4194a9ea3b394ac3dedb1f02021-11-25T05:47:43ZPaternal effect of the nuclear formin-like protein MISFIT on Plasmodium development in the mosquito vector.1553-73661553-737410.1371/journal.ppat.1000539https://doaj.org/article/2f831be0a4194a9ea3b394ac3dedb1f02009-08-01T00:00:00Zhttps://www.ncbi.nlm.nih.gov/pmc/articles/pmid/19662167/?tool=EBIhttps://doaj.org/toc/1553-7366https://doaj.org/toc/1553-7374Malaria parasites must undergo sexual and sporogonic development in mosquitoes before they can infect their vertebrate hosts. We report the discovery and characterization of MISFIT, the first protein with paternal effect on the development of the rodent malaria parasite Plasmodium berghei in Anopheles mosquitoes. MISFIT is expressed in male gametocytes and localizes to the nuclei of male gametocytes, zygotes and ookinetes. Gene disruption results in mutant ookinetes with reduced genome content, microneme defects and altered transcriptional profiles of putative cell cycle regulators, which yet successfully invade the mosquito midgut. However, developmental arrest ensues during the ookinete transformation to oocysts leading to malaria transmission blockade. Genetic crosses between misfit mutant parasites and parasites that are either male or female gamete deficient reveal a strict requirement for a male misfit allele. MISFIT belongs to the family of formin-like proteins, which are known regulators of the dynamic remodeling of actin and microtubule networks. Our data identify the ookinete-to-oocyst transition as a critical cell cycle checkpoint in Plasmodium development and lead us to hypothesize that MISFIT may be a regulator of cell cycle progression. This study offers a new perspective for understanding the male contribution to malaria parasite development in the mosquito vector.Ellen S C BushellAndrea EckerTimm SchlegelmilchDavid GouldingGordon DouganRobert E SindenGeorge K ChristophidesFotis C KafatosDina VlachouPublic Library of Science (PLoS)articleImmunologic diseases. AllergyRC581-607Biology (General)QH301-705.5ENPLoS Pathogens, Vol 5, Iss 8, p e1000539 (2009)
institution	DOAJ
collection	DOAJ
language	EN
topic	Immunologic diseases. Allergy RC581-607 Biology (General) QH301-705.5
spellingShingle	Immunologic diseases. Allergy RC581-607 Biology (General) QH301-705.5 Ellen S C Bushell Andrea Ecker Timm Schlegelmilch David Goulding Gordon Dougan Robert E Sinden George K Christophides Fotis C Kafatos Dina Vlachou Paternal effect of the nuclear formin-like protein MISFIT on Plasmodium development in the mosquito vector.
description	Malaria parasites must undergo sexual and sporogonic development in mosquitoes before they can infect their vertebrate hosts. We report the discovery and characterization of MISFIT, the first protein with paternal effect on the development of the rodent malaria parasite Plasmodium berghei in Anopheles mosquitoes. MISFIT is expressed in male gametocytes and localizes to the nuclei of male gametocytes, zygotes and ookinetes. Gene disruption results in mutant ookinetes with reduced genome content, microneme defects and altered transcriptional profiles of putative cell cycle regulators, which yet successfully invade the mosquito midgut. However, developmental arrest ensues during the ookinete transformation to oocysts leading to malaria transmission blockade. Genetic crosses between misfit mutant parasites and parasites that are either male or female gamete deficient reveal a strict requirement for a male misfit allele. MISFIT belongs to the family of formin-like proteins, which are known regulators of the dynamic remodeling of actin and microtubule networks. Our data identify the ookinete-to-oocyst transition as a critical cell cycle checkpoint in Plasmodium development and lead us to hypothesize that MISFIT may be a regulator of cell cycle progression. This study offers a new perspective for understanding the male contribution to malaria parasite development in the mosquito vector.
format	article
author	Ellen S C Bushell Andrea Ecker Timm Schlegelmilch David Goulding Gordon Dougan Robert E Sinden George K Christophides Fotis C Kafatos Dina Vlachou
author_facet	Ellen S C Bushell Andrea Ecker Timm Schlegelmilch David Goulding Gordon Dougan Robert E Sinden George K Christophides Fotis C Kafatos Dina Vlachou
author_sort	Ellen S C Bushell
title	Paternal effect of the nuclear formin-like protein MISFIT on Plasmodium development in the mosquito vector.
title_short	Paternal effect of the nuclear formin-like protein MISFIT on Plasmodium development in the mosquito vector.
title_full	Paternal effect of the nuclear formin-like protein MISFIT on Plasmodium development in the mosquito vector.
title_fullStr	Paternal effect of the nuclear formin-like protein MISFIT on Plasmodium development in the mosquito vector.
title_full_unstemmed	Paternal effect of the nuclear formin-like protein MISFIT on Plasmodium development in the mosquito vector.
title_sort	paternal effect of the nuclear formin-like protein misfit on plasmodium development in the mosquito vector.
publisher	Public Library of Science (PLoS)
publishDate	2009
url	https://doaj.org/article/2f831be0a4194a9ea3b394ac3dedb1f0
work_keys_str_mv	AT ellenscbushell paternaleffectofthenuclearforminlikeproteinmisfitonplasmodiumdevelopmentinthemosquitovector AT andreaecker paternaleffectofthenuclearforminlikeproteinmisfitonplasmodiumdevelopmentinthemosquitovector AT timmschlegelmilch paternaleffectofthenuclearforminlikeproteinmisfitonplasmodiumdevelopmentinthemosquitovector AT davidgoulding paternaleffectofthenuclearforminlikeproteinmisfitonplasmodiumdevelopmentinthemosquitovector AT gordondougan paternaleffectofthenuclearforminlikeproteinmisfitonplasmodiumdevelopmentinthemosquitovector AT robertesinden paternaleffectofthenuclearforminlikeproteinmisfitonplasmodiumdevelopmentinthemosquitovector AT georgekchristophides paternaleffectofthenuclearforminlikeproteinmisfitonplasmodiumdevelopmentinthemosquitovector AT fotisckafatos paternaleffectofthenuclearforminlikeproteinmisfitonplasmodiumdevelopmentinthemosquitovector AT dinavlachou paternaleffectofthenuclearforminlikeproteinmisfitonplasmodiumdevelopmentinthemosquitovector
_version_	1718414450135924736

Paternal effect of the nuclear formin-like protein MISFIT on Plasmodium development in the mosquito vector.

Ejemplares similares