Rice blast fungus ‘eats’ itself to attack plants

rice blast fungus
© iStock/chirawan

The cells of rice blast fungus endure major changes when it infects its host plant. One of these changes involves using the components of its own cell wall.

In order to response to environmental changes and nutrient starvation, cells are known to undergo severe alterations. This includes switching from one type to another and changes in metabolic pathways.

In a new study, a team of researchers from Tokyo University of Science showed for the first time how rice blast fungus uses its own cell wall to survive in response to certain stimuli.

All living organisms respond and adjust to changes in their environment. These responses are sometimes so significant that they cause alterations in the internal metabolic cycles of the organism—a process called “metabolic switching.”

©Prof Takashi Kamakura

Rice blast fungus, a pathogenic fungal species that causes the “rice blast” infection in rice crops—switches to the “glyoxylate cycle” when the nutrient source starts to deplete. Another response to environmental change is called “cell differentiation”, where cells switch to another type altogether. In rice blast fungus, for example, the fungal cells differentiate and generate a large amount of pressure on the cell wall, causing the fungus to develop a specialised structure called “appressorium,” which ultimately facilitates the infection. Such methods of adaptation have been seen across various organisms, but exactly how they occur is not very clear yet.

In a recent study published in iScience, a team of researchers at Tokyo University of Science, led by Prof Takashi Kamakura, found for the first time that extremely low concentrations of acetic acid alter cellular processes in rice blast fungus.

Their research was based on the fact that Cbp1—a protein that can remove acetyl groups from chitin (the main component of the cell wall of fungi)—plays a huge role in appressorium formation by converting chitin into chitosan and releasing acetic acid.

Explaining the objective of the study, Kamakura says, “Metabolic switching in nutrient-deficient environments depends on changes in the nutrient source, but its mechanism has remained poorly understood until now. Since chitin was known to induce a subsequent resistance response (immune response), we speculated that Cbp1 functions to escape recognition from plants. Also, because the enzymatic activity of Cbp1 affects cell differentiation, we hypothesised that the reaction product of chitin deacetylation by Cbp1 may be a signal for cell differentiation.”


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