日時
2026年9月7日(月)14:00 - 15:00 (JST)
講演者
  • 熊倉 直祐 (理化学研究所 環境資源科学研究センター (CSRS) 上級研究員)
言語
英語
ホスト
Kyosuke Adachi

Many devastating crop diseases, including anthracnose and rice blast, begin when a fungal pathogen builds a single infection cell called an appressorium. This single cell generates up to ~8 megapascals of turgor pressure (roughly 40 times a car tire’s air pressure), among the highest documented in any living organism, to physically rupture the plant's tough surface. This pressure arises because the cell wall acts as a semipermeable membrane, retaining internal osmolytes such as glycerol while allowing water to pass. What confers this selective permeability had remained unknown for decades: melanin was long assumed responsible, but turgor still forms in melanin-deficient mutants.

Using genome editing and direct biochemical analysis of these fungi, we identified two enzymes, PKS2 and PBG13, that synthesize a novel polymer from dihydroxyhexanoic acid (DHHA), which narrows cell-wall pore size at the nanometer scale and is required for turgor generation (Kumakura* et al., Science, 2026). I will frame this system as a living adaptive porous material and discuss questions open to mathematical and physical modeling, including how pore geometry sets the limits of selective permeability.

Reference

  1. Kumakura* et al., Dihydroxyhexanoic acid biosynthesis controls turgor in pathogenic fungi, Science 391, 700-706 (2026), doi: 10.1126/science.aec9443

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