10.1371/journal.pone.0150172
Pedro J. Alcolea
Pedro
J. Alcolea
Ana Alonso
Ana
Alonso
Miguel A. Moreno-Izquierdo
Miguel
A. Moreno-Izquierdo
María A. Degayón
María
A. Degayón
Inmaculada Moreno
Inmaculada
Moreno
Vicente Larraga
Vicente
Larraga
Serum Removal from Culture Induces Growth Arrest, Ploidy Alteration, Decrease in Infectivity and Differential Expression of Crucial Genes in <i>Leishmania infantum</i> Promastigotes
Public Library of Science
2016
promastigote development
Serum deprivation
HASPB
Axenic cultures
amastin gene
Mediterranean basin
culture media
growth rate decreases
Crucial Genes
GLO
Leishmania infantum Promastigotes Leishmania infantum
surface protein B
Leishmania spp
Ploidy Alteration
infectivity
species
FAS
Culture Induces Growth Arrest
Differential Expression
Serum Removal
growth kinetics
GINS
expression rate
MMCE
2016-03-09 08:33:41
Dataset
https://plos.figshare.com/articles/dataset/Serum_Removal_from_Culture_Induces_Growth_Arrest_Ploidy_Alteration_Decrease_in_Infectivity_and_Differential_Expression_of_Crucial_Genes_in_i_Leishmania_infantum_i_Promastigotes/3105526
<div><p><i>Leishmania infantum</i> is one of the species responsible for visceral leishmaniasis. This species is distributed basically in the Mediterranean basin. A recent outbreak in humans has been reported in Spain. Axenic cultures are performed for most procedures with <i>Leishmania</i> spp. promastigotes. This model is stable and reproducible and mimics the conditions of the gut of the sand fly host, which is the natural environment of promastigote development. Culture media are undefined because they contain mammalian serum, which is a rich source of complex lipids and proteins. Serum deprivation slows down the growth kinetics and therefore, yield in biomass. In fact, we have confirmed that the growth rate decreases, as well as infectivity. Ploidy is also affected. Regarding the transcriptome, a high-throughput approach has revealed a low differential expression rate but important differentially regulated genes. The most remarkable profiles are: up-regulation of the GINS Psf3, the fatty acyl-CoA synthase (FAS1), the glyoxylase I (GLO1), the hydrophilic surface protein B (HASPB), the methylmalonyl-CoA epimerase (MMCE) and an amastin gene; and down-regulation of the gPEPCK and the arginase. Implications for metabolic adaptations, differentiation and infectivity are discussed herein.</p></div>