ÿþ<HTML><HEAD><TITLE>XI International Meeting on Paracoccidioidomycosis</TITLE><link rel=STYLESHEET type=text/css href=css.css></HEAD><BODY aLink=#ff0000 bgColor=#FFFFFF leftMargin=0 link=#000000 text=#000000 topMargin=0 vLink=#000000 marginheight=0 marginwidth=0><table align=center width=700 cellpadding=0 cellspacing=0><tr><td align=left bgcolor=#cccccc valign=top width=550><font face=arial size=2><strong><font face=Verdana, Arial, Helvetica, sans-serif size=3><font size=1>XI International Meeting on Paracoccidioidomycosis</font></font></strong><font face=Verdana size=1><b><br></b></font><font face=Verdana, Arial,Helvetica, sans-serif size=1><strong> </strong></font></font></td><td align=right bgcolor=#cccccc valign=top width=150><font face=arial size=2><strong><font face=Verdana, Arial, Helvetica, sans-serif size=1><font size=1>Resume:93-1</font></em></font></strong></font></td></tr><tr><td colspan=2><br><br><table align=center width=700><tr><td><b>Poster (Painel)</b><br><table width="100%"><tr><td width="60">93-1</td><td><b>Autophagy in Paracoccidioides brasiliensis during mycelium to yeast transition</b></td></tr><tr><td valign=top>Authors:</td><td>Sarah Pedroso (UNIVAP - UNIVERSIDADE DO VALE DO PARAIBA) ; Claudia Campos (UNIVAP - UNIVERSIDADE DO VALE DO PARAIBA) ; <u>Flavia Morais </u> (UNIVAP - UNIVERSIDADE DO VALE DO PARAIBAUNIP - UNIVERSIDADE PAULISTA) </td></tr></table><p align=justify><b><font size=2>Abstract</font></b><p align=justify class=tres><font size=2>Autophagy is a highly conserved eukaryotic process which allows cells to degrade macromolecules and organelles through the action of lysosomal/vacuole compartments. This process is involved in many biological events such as development, differentiation and adaptation, being crucial for survival of several microorganisms exposed to stress conditions. The human pathogenic fungus <i>Paracoccidioides brasiliensis</i>, the etiological agent of a deep mycosis, paracoccidioidomycosis, needs to undergo mycelium to yeast dimorphism inside the host to establish disease, which is triggered by a thermal stress when fungus changes from 25Ã °C to 37Ã ºC. In <i>P. brasiliensis</i>, many genes involved in autophagy undergo expression induction/repression during mycelium to yeast transition, which may be related to adaptation of the fungus to human host environment. In this work, <i>P. brasiliensis</i>, isolate 18, were cultivated in liquid medium after temperature shift from 25Ã °C to 36Ã °C for 7 days, in presence or absence of the drugs N-ethylmaleimide or 3-methyladenine, two inhibitors of autophagy, in order to establish the involvement of this process during dimorphism. <i>P. brasiliensis</i> mycelia cells cultivated at 25Ã °C during 7 days did not exhibit autophagic vacuoles in presence of monodansylcadaverine, a specific <i>in vivo</i> marker for autophagic vacuoles. However, the temperature rise from 25Ã °C to 37Ã °C in the presence of monodansylcadaverine, induced abundant autophagic vacuoles in <i>P. brasiliensis</i> cells during the first 24 hours. Both N-ethylmaleimide and 3-methyladenine blocked the mycelium to yeast transition by either death or stagnation of the culture, respectively. When 3-methyladenine was used, few autophagic vacuoles could be observed by monodansylcadaverine staining. These results suggest that autophagy is involved in <i>P. brasiliensis</i> dimorphism, which could mean that this process might be also involved in <i>P. brasiliensis</i> pathogenicity and virulence. Supported by Fapesp. </font></p><br><b>Keyword: </b>&nbsp;autophagy, dimorphism, pathogenicity</td></tr></table></tr></td></table></body></html>