
Projekte
Moleculare Mycology und Mycoparasitism
HIPSTeR: Host-Induced Polarity Stress Response
Dissecting the SAPK/GTPase signalling network that regulates adaptive recovery from host-induced polarity stress in Trichoderma atroviride
Filamentous fungi of the genus Trichoderma are powerful mycoparasites that kill plant pathogenic fungi and are therefore applied for crop plant protection as so-called biocontrol agents in agriculture. HIPSTeR builds on the novel phenomenological insights of T. tip and investigates the molecular mechanisms that control fungus-fungus interactions between the mycoparasite Trichoderma atroviride and plant pathogenic host fungi.

Our current investigations indicate that T. atroviride exploits cell polarity stress signals, elicited by host defence responses to stop the mycoparasitic attack, to rapidly re-polarise and switch to a new aggressive growth strategy to target the host. This is unusual because hyphae normally avoid the stress stimulus and promote growth elsewhere. The comparison of different host species, however, suggests that Trichoderma utilises stress signalling to adapt its growth morphology in a host-specific way.
The role of stress-activated protein kinase (SAPK)/GTPase signalling suspected to underlie this phenomenon is well established during normal growth in non-mycoparasitic species, but the differential control required for mycoparasitism has not yet been determined for any species. We predict an ‘actin-stress response’ in which SAPKs elicit negative feedback on GTPase cluster maintenance resulting in rapid F-actin disassembly and loss of tip polarity. Actin monomers in turn activate MAPKs that shut down SAPKs to allow equally rapid repolarisation via polarity markers that initiate stress-adapted recovery of tip growth.

The three hypotheses HIPSTeR will test are: (1) T. atroviride employs an ‘actin stress response’ to sense and adapt to host-induced polarity stress; (2) Polarity markers are left behind that allow GTPase cluster reassembly and rapid repolarisation near the previous growth axis; and (3) SAPK/GTPase pathway rewiring will desensitise T. atroviride towards host-defence responses and trigger hyperparasitic growth.
The approach HIPSTeR will take to dissect the SAPK/GTPase signalling network of T. atroviride is to systematically characterise the intracellular recruitment dynamics of GTPase activity clusters relative to the dynamics and activity of putative SAPKs and MAPKs.

This will be accomplished by generating a set of monospecific GTPase biosensors (CRIB reporter, uniquely used for filamentous fungi in our lab) and their coexpression with the Lifeact F-actin reporter and fluorescently labelled SAPK and MAPK fusion proteins. Pharmacogenetic and optogenetic approaches in combination with advanced live-cell imaging microscopy and custom build automated image analysis software will provide a versatile molecular tool kit to interrogate protein functions and to build the SAPK/GTPase network map out of 25 primary target proteins.
HIPSTeR will deliver fundamentally new insights into cell polarity stress regulation and provide the first functional link between microparasitic and macroparasitic features of mycoparasitism.