How Does the Botrytis Fungus Kill Plant Cells?

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How does the Botrytis fungus kill plant cells? It does not rely on a single method. Botrytis cinerea is a necrotrophic pathogen, which means it kills host cells in order to reach their nutrients. Its attack combines acids, reactive oxygen, cell wall degrading enzymes and toxins. The second source also shows that one secreted fungal protein, BcCDI1, can switch on plant cell death. This article walks through each part of the process in order and marks where the sources stop.

Quick answer

• The fungus kills host cells to access nutrients, which is what makes it a necrotrophic pathogen.
• It secretes oxalic acid, cell wall degrading enzymes, reactive oxygen and toxins that damage host tissue.
• The secreted protein BcCDI1 can induce plant cell death through a plant protein the study has not identified.
• The sources do not describe every step inside a single infected cell.

What Botrytis cinerea is

Botrytis cinerea is a fungus that causes gray mold and rot. The second source describes it as “a necrotrophic fungus and typical broad host-range phytopathogen, which leads to gray mold and rot diseases in a wide range of agriculturally important crops, causing severe economic loss worldwide.” The first source gives the general rule for the genus: “Members of Botrytis genus are generally necrotrophic pathogens; they induce host cell death and lysis to access cellular nutrients.” The word necrotrophic describes the feeding strategy. The fungus causes the death of host tissue, and then it draws on the contents of those cells. That is why cell death is central to how the fungus feeds.

How infection begins

The first source describes the early stage in two sentences: “B. cinerea mostly initiates infection through conidia spores landing on host plants. They germinate and form appressoria used for host tissue penetration.” The appressoria are the structures the fungus uses to get into plant tissue. The same source says that “Evading host immunity and production of molecules leading to host cell death are key invasion strategies in B. cinerea.” That sentence links the start of infection to the chemical attack that follows. The sources give less detail on the entry step than on the later damage, so this article focuses on the damage. For a separate look at leaf pores, see how do stomata open and close.

Acids, reactive oxygen and toxins

Once inside, the fungus releases a mix of chemicals. The first source lists the virulence factors as “oxalic acid (OA), cell wall degrading enzymes (CWDEs) and analogues of plant hormones,” and says the fungus secretes them “to disrupt host metabolism, immune system and cellular structure.” Oxalic acid is one of the acids in this group. The review’s summary of the damage is short: “Degradation of plant tissues is achieved via the production of acids, ROS, CWDEs and compound appressoria and inducing plant cell death.”

Reactive oxygen is the second group. The review says that “After penetration, B. cinerea secretes numerous virulence factors to induce host cell damage and necrosis. Generally, these factors include ROS and fungal toxins.” One example is an enzyme pair: “The two H 2 O 2 generating enzymes in B. cinerea are Cu-Zn-superoxide dismutase SOD1 and glucose oxidase GOD1.” Of these, the review reports that “sod1 deletion mutants exhibited significantly retarded lesion development, indicating that SOD1 is a key gene in H 2 O 2 generation.” The same passage notes that “god1 mutants had no observable phenotypic change”, so the two enzymes do not play equal roles in lesion growth.

Toxins form the third group. The review says the fungus “can potentially produce over 40 different SM, including sesquiterpene botrydial and polyketide botcinic acid phytotoxins.” In one mutant strain described in the review, the mycelium “could penetrate host tissue but was unable to produce lesions,” and the authors suspect that “the inability to cause lesions is due to the loss of phytotoxin production.” The review presents this as a suspicion rather than a confirmed mechanism, and this article treats it the same way.

Cell wall enzymes break down the tissue

Plant cell walls are a barrier, and the fungus carries enzymes that attack them. The first source describes a genome annotation that found “a wide diversity of 229 different CAZymes, likely responsible for the decomposition of pectin, hemicellulose and cellulose in plant cell walls.” The word “likely” signals a prediction from the genome rather than a measured result for each enzyme. The review also groups the cell wall degrading enzymes with the other factors that break down host tissue, which is the same list quoted earlier.

Effector proteins can trigger cell death

The second source studies one protein, BcCDI1, which belongs to the group of “Cell death-inducing proteins (CDIPs).” Its introduction gives the broader context: “Since B. cinerea achieves its infection and colonization by killing plant cells, it secretes diverse effector proteins to manipulate the host defense and/or induce necrosis to facilitate its infection on the host plants.” The study reports that “the secreted protein BcCDI1 (Cell Death Inducing 1) can cause necrosis in tobacco leaves and at the same time elicit plant defense.” Its mechanism is described this way: “Further analysis demonstrated that BcCDI1 can induce plant cell death by interacting with an unknown RLP in the apoplastic space of plant cells.”

The study also tested which plant proteins are needed. It reports that “the plant receptor-like kinases BAK1 and SOBIR1 are required to transduce the cell death-promoting signal induced by BcCDI1.” The authors conclude that “Our results demonstrated that BcCDI1 is an apoplast-localized CDIP, and its necrosis-inducing activity is dependent on NbBAK1/NbSOBIR1 and possibly mediated by an unknown RLK or RLP.” In plain terms, the signal depends on two plant proteins, and the receptor that starts it is not identified in the source. The study also reports that the protein “could also trigger cell death in tomato and potato leaves,” so its effect is not limited to tobacco.

The plant side of this interaction is also complicated. The second source explains that “However, HR and the related programmed cell death (PCD) of plants are ineffective for necrotrophic pathogens, and necrotrophs can even exploit the HR and PCD to facilitate their infection.” In other words, the plant’s own cell death response does not stop this kind of fungus, and the fungus can turn that response to its advantage.

Why cell death helps the fungus

The second source states the logic of the attack: “It has been demonstrated that the successful establishment of pathogen infection largely depends on the killing of a sufficient number of host cells to create a region of dead plant tissue, in which fungal biomass will be accumulated before the transition to the intermediate and then late infection phases.” The phrase “region of dead plant tissue” describes the space the fungus needs before it can grow in number. The first source explains what happens next: “Upon killing the host tissue, B. cinerea can continue to grow saprophytically within the plant remains in the form of sclerotia and mycelia.” The same source adds that “The sclerotia of B. cinerea are highly resistant to environmental changes.” It also describes spread: “adjacent plant tissue may become infected, allowing for the spread of grey mold across the whole plant and to plants nearby.”

How we chose the sources

The two sources cover different levels of the problem. The first is a review of Botrytis cinerea genes studied through mutant analysis. The second is a research study of one secreted protein. Both were opened from the PubMed Central archive, which describes itself with the line “As a library, NLM provides access to scientific literature.” Neither source is a retail page, and both were selected for their mechanism content. For a related plant pathogen topic, readers can see how does phytophthora spread through soil.

What we could not verify

The sources answer the question in outline but leave several steps open. The first source notes that “With almost 11,000 genes encoded in its genome, only less than 150 genes have been genetically studied so far through mutant analysis.” That is a large gap, and it limits how much detail any single review can give about the killing process. Some points in this article therefore rest on a single source. The article keeps those points short rather than filling them with general statements.

What the sources do not say

The sources do not describe how oxalic acid, reactive oxygen or the toxins damage an individual plant cell at the molecular level. The review names oxalic acid among the virulence factors, but the text does not explain its effect on a single cell. The second source describes the receptor for BcCDI1 only as an unknown RLP, so the exact plant receptor is not identified. The study also reports that “Our results demonstrate that the BcCDI1 gene does not affect the outcome of B. cinerea infection,” which means this one protein is not the whole answer to how the fungus kills cells.

Frequently asked questions

Is Botrytis cinerea a necrotrophic fungus?

Yes. The second source calls it “a necrotrophic fungus and typical broad host-range phytopathogen.” Necrotrophs kill host tissue to feed, and the first source describes the genus this way: they “induce host cell death and lysis to access cellular nutrients.”

Does the fungus kill plant cells before it feeds on them?

According to the first source, the fungus induces “host cell death and lysis to access cellular nutrients.” Cell death comes first in that description, and access to the cell contents follows.

What chemicals does Botrytis use to damage plant tissue?

The first source lists oxalic acid, cell wall degrading enzymes, reactive oxygen species and fungal toxins among its tools. It names “sesquiterpene botrydial and polyketide botcinic acid phytotoxins” as examples of the toxins it can produce.

Can a single fungal protein make plant cells die?

In the second source, the protein BcCDI1 causes necrosis in tobacco leaves and can induce plant cell death through a plant protein the study has not identified. The same study reports that “Our results demonstrate that the BcCDI1 gene does not affect the outcome of B. cinerea infection,” so according to that study, the gene does not change the outcome of infection.

Does gray mold keep spreading after the host dies?

The first source says that “adjacent plant tissue may become infected, allowing for the spread of grey mold across the whole plant and to plants nearby.” It also says that “Upon killing the host tissue, B. cinerea can continue to grow saprophytically within the plant remains in the form of sclerotia and mycelia.” The review does not give a time frame for either process.

Sources

• The Destructive Fungal Pathogen Botrytis cinerea: Insights from Genes Studied with Mutant Analysis (review, PubMed Central), https://pmc.ncbi.nlm.nih.gov/articles/PMC7695001/ (HTTP 200, opened 2026-10-28)
• Botrytis cinerea BcCDI1 protein triggers both plant cell death and immune response (research article, PubMed Central), https://pmc.ncbi.nlm.nih.gov/articles/PMC10167277/ (HTTP 200, opened 2026-10-28)