A fungus that leaves a familiar grey fuzz on strawberries, tomatoes and grapes has long frustrated farmers and plant breeders because it infects an unusually wide range of crops while repeatedly overcoming efforts to breed durable resistance. Two complementary studies have now shown that the pathogen succeeds because neither it nor its host follows a fixed playbook. Instead, both continuously adjust their genetic responses during infection.

The studies, published in the Proceedings of the National Academy of Sciences (PNAS), examined the fungal pathogen Botrytis cinerea, commonly known as grey mold. The fungus infects more than 1,500 plant species, causing major losses in fruits, vegetables, ornamentals and field crops both before harvest and during storage.

For decades, scientists assumed that B. cinerea, a so-called generalist pathogen, relied on essentially the same infection mechanism regardless of the plant it attacked. Crop breeding programmes therefore searched for resistance genes that could provide broad protection against the fungus.

The new findings challenge that assumption.

Researchers at the Department of Plant Sciences, University of California, Davis, analysed gene activity in both the fungus and its host plants across multiple crop species and fungal isolates. They found that disease results from a dynamic interaction in which the pathogen modifies its infection strategy while the plant mounts a defence response that is unique to that particular encounter.

The first study shows that the fungus employs a modular infection strategy. One set of genes remains active across all hosts and carries out core functions essential for infection, including metabolism and lesion formation. Alongside this conserved programme is another set of genes that switches on only after the fungus recognises the particular plant it is infecting.

“It is almost as if the pathogen first activates a broad infection response, then starts reading the plant in front of it and activates its weapons accordingly,” said Ritu Singh, Postdoctoral Scholar at the University of California, Davis, and first author of the studies.

This flexibility appears to explain why grey mold can infect crops as diverse as tomato, lettuce, sunflower, bean and grape instead of relying on a single universal mechanism. The work also indicates that broad host range depends less on acquiring new genes than on changing when and where existing genes are activated.

The second study turned the focus to the plants.

Contrary to the long-held view that different plant species respond similarly to a common pathogen, the researchers found that each host activates a distinct genetic defence programme. Even closely related plants that develop similar disease symptoms often rely on entirely different sets of genes to produce those responses.

The study also found that the plant’s defence depends on the particular fungal isolate involved. Different isolates of B. cinerea triggered different defence responses in the same plant, suggesting that resistance observed under laboratory conditions may not hold up in farmers’ fields, where genetically diverse fungal populations coexist.

“Everyone had theories about how Botrytis might infect diverse hosts, but there was little data that could be directly compared across different host plants and fungal isolates,” said Daniel J. Kliebenstein, professor at the University of California, Davis, who led the research. “We designed an experiment that allowed us to compare infection mechanisms and gene activity across both hosts and pathogen isolates, enabling these ideas to be tested.”

Together, the studies suggest that grey mold is not a single disease governed by one molecular mechanism. Rather, every infection represents a unique combination of plant genetics and fungal variation.

The findings also have implications for crop improvement. Instead of searching for universal resistance genes that can be transferred across species, breeders may need to account for the genetic diversity present in both crop plants and pathogen populations. Conserved fungal genes identified in the study could provide targets for developing broader disease-control strategies.

The researchers are now investigating how the fungus recognises the host before altering its infection programme.

“The next work is focused on how the fungus detects the specific hosts it is on,” Prof. Kliebenstein said. “By finding these genes, we would have fungal targets that could be altered through molecular biology or chemistry, allowing the plant’s own defences to defeat the fungus.”

If successful, disrupting this host-sensing mechanism could open a new route to protecting a wide range of economically important crops from one of agriculture’s most persistent fungal pathogens.

The studies were conducted by Ritu Singh, Anna Jo Muhich, Cloe Tom, Celine Caseys, Jack McMillan, Karishma Srinivas, Lucca Faieta, and Daniel J. Kliebenstein, all from the Department of Plant Sciences at the University of California, Davis.