Infecting a maize plant is no simple task for a fungal pathogen such as Ustilago maydis . A group of researchers led by Heinrich Heine University Düsseldorf (HHU) has now uncovered how the fungus detects that it has successfully entered its host. This signal triggers changes in fungal growth, as the researchers report in the scientific journal Nature Communications .
The fungus Ustilago maydis infects maize plants and causes corn smut. The disease produces large galls, particularly on maize cobs, in which the fungus forms spores. Dr Florian Altegoer leads a research group at the Institute of Microbiology at HHU, which is investigating the mechanisms underlying fungal infection.
To establish an infection, the fungus must penetrate plant tissue and manipulate the host’s growth. In order to colonise the host cell successfully, Ustilago maydis must also recognise when it has reached the environment inside the plant so that it can adjust its physiology and begin proliferating.
Altegoer and his team investigated how the corn smut fungus senses its arrival inside plant tissue and translates this signal into changes in growth. Researchers from the University of Göttingen, North Carolina State University in the USA and Imperial College London were also involved in the work.
At the centre of the study is Gpe1, a receptor located in the fungal cell membrane. Gpe1 belongs to a family of proteins known as G protein-coupled receptors (GPCRs). These receptors have been studied extensively in humans and are important targets for many medicines. Much less is known about their functions in fungi.
“We have identified a previously unknown fungal GPCR and uncovered an unusual mechanism by which it is activated,” says Altegoer: During infection, the fungus secretes the protein Pit2 into its immediate surroundings. Hidden within Pit2 is a short peptide. Once the fungus enters plant tissue, plant enzymes cleave Pit2 and release the peptide, which then activates Gpe1.
“The fungus thus ironically utilises enzymes from its host plant to detect that it has entered the tissue successfully,” says Gabriel Mendoza-Rojas, member of Altegoer’s group and lead author of the study, which has now been published in Nature Communications: “This is also reflected in the molecular structure of the surrounding material: The peptide is hidden inside Pit2, like treasure in a chest that only plant enzymes can open. However, opening this chest is more like opening Pandora’s box: It releases a signal that benefits the fungus at the plant’s expense.”
Activation of Gpe1 promotes fungal proliferation. The researchers found that the fungal cell cycle becomes significantly shorter. They also observed the production of Clp1, a cell-cycle regulator associated with the resumption of fungal cell division, following host entry. “Our work establishes a mechanistic link between sensing the host environment and resuming fungal proliferation after entry,” says Altegoer.
The system is also noteworthy from an evolutionary point of view. The researchers found indications that Gpe1 and Pit2 co-evolved, as the receptor and signalling protein seem to be closely coordinated. The team now plans to investigate how widespread similar signalling systems are among fungi. “We want to find out whether other fungi use comparable receptors to sense their surroundings and adjust their growth,” says Altegoer.
The findings may also have broader implications, as GPCRs are an important family of cellular signalling proteins. In the longer term, a better understanding of fungal GPCRs could reveal new ways to selectively influence the growth of pathogenic fungi.
Receptors are proteins that recognise specific molecules known as ligands. Their binding sites are precisely matched and thus often compared to locks that only fit particular keys. When a ligand binds, the receptor triggers a defined signal inside the cell, which can regulate other processes.
Gabriel Mendoza-Rojas, Philip Nakonz, Min Lu, Nora Marie Kühne, Johannes Postma, Naomi Shtakser, Max Heinen, Manav Patel, Orlando Arguello-Miranda, Kai Heimel, Sonja Billerbeck and Florian Altegoer. A co-evolved peptide-GPCR system senses host entry to drive fungal infection. Nature Communications (2026)
DOI: 10.1038/s41467-026-78428-6
Nature Communications
A co-evolved peptide-GPCR system senses host entry to drive fungal infection
9-Oct-2026