A specialized fungal metabolite plays a structural role in turgor generation and host plant penetration

Devastating phytopathogenic fungi such as Colletotrichum and Magnaporthe penetrate their host plants through the mechanical force exerted by specialized infection cells known as appressoria. A study published in Science, conducted within an international consortium coordinated by Dr. Naoyoshi Kumakura of the RIKEN Institute (Center for Sustainable Resource Science, Yokohama, Japan), and involving researchers from the BIOGER unit (UPSaclay/INRAE) and the Institut des Sciences Moléculaires d'Orsay (UPSaclay/CNRS), elucidated the molecular mechanism by which appressoria generate the enormous turgor pressure (37 atmospheres) required for host penetration.

It has long been established that appressorial turgor generation requires both the accumulation of osmolytes in the cytosol and a semi-permeable cell wall; however, the molecular determinants of this permeability barrier remained unknown. Using a reverse genetics approach, the researchers identified two enzymes— the polyketide synthase PKS2 and the hydrolase PBG13— as essential for both pathogenicity and the formation of this semi-permeable barrier in Colletotrichum and Magnaporthe. The compounds synthesized by these enzymes were shown to be polymers of 3,5-dihydroxyhexanoic acid (DHHA), which accumulate in the appressorial cell wall, where they apparently reduce pore size, thereby contributing to turgor generation.

Until now, melanin— a polymer derived from 1,8-dihydroxynaphthalene and present in the cell wall— was considered the sole component required for turgor generation in appressoria. Comparison of melanin- or DHHA-deficient mutants revealed that, whereas melanin strengthens the cell wall to withstand high turgor pressure, DHHA polymers establish a semi-permeable barrier that prevents osmolyte leakage. This study highlights new potential targets for disease control.

Regulation of turgor by PKS2 and PBG13

(A) In pks2 or pbg13 mutants, cell wall porosity is increased due to the absence of DHHA polymers.
(B) TEM analysis of Chpks2 appressoria reveals alterations in cell wall structure.
(C) FLIM analysis using the Flipper tension probe reflects changes in membrane tension in Chpks2 appressoria.

See publication : www.science.org february 12, 2026. 

 Contact : richard.oconnell@inrae.fr; Julien.pernier@inrae.fr; sandrine.leveque-fort@cnrs.fr