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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.




Chemical tug-of-war between mycoparasite and prey fungus. (A) Before Botrytis cinerea (expressing cytoplasmic GFP) is chemically attacked by T. atroviride, the apical cell wall extends quickly and hence shows only weak staining with the chitin-specific fluorescent dye Congo Red (CR, arrowheads). (B) As soon as chemical attack takes effect, hyphal tip growth arrests, leading to tip swelling and increased deposition of chitin in the apical cell wall (arrowheads). (C) Eventually, tip lysis of the prey hypha results in the release of cytoplasm into the surrounding (asterisks), which serves the mycoparasite as nutrient substrate. (D) Fluorescent reporters of polarised tip growth (CRIB reporter generated in T.tip) show that normal tip growth of T. atroviride hyphae (left inset) is in turn affected by the presence of the prey fungus B. cinerea (expressing cytoplasmic RFP, right inset). Because this effect occurs exclusively in near proximity to the prey, it is very likely the result of its defence response. The three dots indicate the larger distance between these two regions of the montaged sample.


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.




Stress-response pathway in S. cerervisiae. (A) Osmotic stress is perceived through the HOG MAPK pathway employing the MAPK Hog 1 as SAPK, and leads to cell cycle arrest and F-actin disassembly. (B) In turn, binding of actin monomers to the regulatory domain of the HOG MAP3K Ssk2 triggers polarisome-mediated F-actin reassembly. Images taken from Amberg lab homepage at Upstate Medical University, New York. Subsequent research showed that crosstalk with MAPKs of the CWI pathway occupies the positions indicated by (?) en route to actin recovery.


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.




Cdc42 activity clusters form by positive feedback. (A) The PAK-Bem1-Cdc24 complex activates Cdc42 at the plasma membrane. (B) Assembly of more polarity components enlarges the cluster. (C) Targeted secretion along efferent F-actin cables protrudes the cell cortex (from (Chiou et al. 2017)).


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.


Group members

Alexander LichiusAlexander Lichius, PI

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International CollaboratorUniversity of Oxford

Mark FrickerMark Fricker

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