Specialising the parasite nucleus: Pores, lamins, chromatin, and diversity

TY - JOUR

T1 - Specialising the parasite nucleus

T2 - Pores, lamins, chromatin, and diversity

AU - Rout, Michael P.

AU - Obado, Samson O.

AU - Schenkman, Sergio

AU - Field, Mark C.

N1 - Work in the authors’ laboratories is supported by MR/N010558/1, MR/K008749/1, MR/P009018/1 from the MRC and Investigator award 204697/Z/16/Z from the Wellcome Trust and NIH (nih.gov) (P41 GM109824, R01 GM112108 and R21 AI096069 to MPR), and Fundação de Amparo à Pesquisa do Estado de São Paulo (http://www.fapesp.br) (11/51973-3, 2015/22031-0 and 2014/50824-91 to SS). The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.

PY - 2017/3/2

Y1 - 2017/3/2

N2 - Infection by protozoan parasites remains a major cause of global human morbidity and economic hardship. With annual death rates exceeding a million people and even higher numbers afflicted by disability and compromised agricultural productivity, the organisms causing tropical diseases like leishmaniasis, trypanosomiasis, malaria, and toxoplasmosis represent an ongoing challenge. Whilst new compounds to treat malaria and toxoplasmosis have been discovered and deployed recently, this progress has not been mirrored for trypanosomiasis or leishmaniasis. Climate change, increased mobility, and mass migration also undermine our ability to control diseases caused by these organisms, and the need for new drugs to combat resistance and new strains of parasites remains acute. Nonetheless, considerable advances in understanding the cell biology of all of these infectious agents have been made, and this new knowledge is poised to contribute strongly to control strategies. In this short article, we will focus on the nuclear biology of trypanosomatid and Apicomplexan parasites, highlighting aspects that appear to represent potentially key adaptations that facilitate infection and, thus, the disease burden of these old enemies.

AB - Infection by protozoan parasites remains a major cause of global human morbidity and economic hardship. With annual death rates exceeding a million people and even higher numbers afflicted by disability and compromised agricultural productivity, the organisms causing tropical diseases like leishmaniasis, trypanosomiasis, malaria, and toxoplasmosis represent an ongoing challenge. Whilst new compounds to treat malaria and toxoplasmosis have been discovered and deployed recently, this progress has not been mirrored for trypanosomiasis or leishmaniasis. Climate change, increased mobility, and mass migration also undermine our ability to control diseases caused by these organisms, and the need for new drugs to combat resistance and new strains of parasites remains acute. Nonetheless, considerable advances in understanding the cell biology of all of these infectious agents have been made, and this new knowledge is poised to contribute strongly to control strategies. In this short article, we will focus on the nuclear biology of trypanosomatid and Apicomplexan parasites, highlighting aspects that appear to represent potentially key adaptations that facilitate infection and, thus, the disease burden of these old enemies.

U2 - 10.1371/journal.ppat.1006170

DO - 10.1371/journal.ppat.1006170

M3 - Article

C2 - 28253370

SN - 1553-7366

VL - 13

SP - 1

EP - 16

JO - PLoS Pathogens

JF - PLoS Pathogens

IS - 3

M1 - e1006170

ER -