Acute inactivation of the <i> <scp>A</scp> spergillus nidulans </i>   <scp>G</scp> olgi membrane fusion machinery: correlation of apical extension arrest and tip swelling with cisternal disorganization

<jats:title>Summary</jats:title> <jats:p> The mechanisms governing traffic across the <jats:styled-content style="fixed-case">G</jats:styled-content> olgi are incompletely understood. We studied, by live‐cell microscopy, the consequences of disorganizing the <jats:italic> <jats:styled-content style="fixed-case">A</jats:styled-content> spergillus nidulans </jats:italic>   <jats:styled-content style="fixed-case">G</jats:styled-content> olgi, using an extended set of fluorescent protein markers to resolve early from late cisternae. The early <jats:styled-content style="fixed-case">G</jats:styled-content> olgi syntaxin <jats:styled-content style="fixed-case"> SedV <jats:sup>Sed</jats:sup> </jats:styled-content> <jats:sup>5</jats:sup> and the <jats:styled-content style="fixed-case"> RabO <jats:sup>Rab</jats:sup> </jats:styled-content> <jats:sup>1</jats:sup> regulatory <jats:styled-content style="fixed-case">GTPase</jats:styled-content> play essential roles in secretion, cooperating in the <jats:styled-content style="fixed-case">ER</jats:styled-content> – <jats:styled-content style="fixed-case">G</jats:styled-content> olgi interface. Following a temperature shift‐up ‘on‐the‐stage’, hyphae carrying engineered <jats:styled-content style="fixed-case"> <jats:italic> sedV <jats:sup>R258G</jats:sup> </jats:italic> </jats:styled-content> and <jats:styled-content style="fixed-case"> <jats:italic> rabO <jats:sup>A136D</jats:sup> </jats:italic> </jats:styled-content>   <jats:italic>ts</jats:italic> mutations arrest polarized growth. This arrest correlates with overall <jats:styled-content style="fixed-case">G</jats:styled-content> olgi disorganization and characteristic hyphal tip swelling. Using v‐ <jats:styled-content style="fixed-case">SNARE SynA</jats:styled-content> as reporter, we show that the <jats:styled-content style="fixed-case"> <jats:italic> sedV <jats:sup>R258G</jats:sup> </jats:italic> </jats:styled-content> phenotypes correlate with arrested secretion. Both the morphogenetic defect and the secretory deficit are reversible. Thus downregulation of secretion, like that of endocytosis, has morphogenetic consequences, implying that mechanisms tuning the secretory pathway might be involved in developmental processes. According to the cisternal maturation model, acute impairment of traffic in the <jats:styled-content style="fixed-case">ER</jats:styled-content> – <jats:styled-content style="fixed-case">G</jats:styled-content> olgi interface should lead to disorganization of both the early and the late <jats:styled-content style="fixed-case">G</jats:styled-content> olgi cisternae. Thus, the relatively rapid late <jats:styled-content style="fixed-case">G</jats:styled-content> olgi disorganization observed upon shifting <jats:styled-content style="fixed-case">ER</jats:styled-content> – <jats:styled-content style="fixed-case">G</jats:styled-content> olgi interface mutants to the restrictive temperature seems incompatible with an <jats:italic> <jats:styled-content style="fixed-case">A</jats:styled-content> . nidulans </jats:italic>   <jats:styled-content style="fixed-case">G</jats:styled-content> olgi network organized on the basis of stable early and late compartments, supporting instead cisternal maturation. </jats:p>