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>