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Scientists unravel DNA sequence of pathogenic fungus that destroys chillies

Read time: 3 mins

Illustration : Balraj K N

 

The hot and spicy chillies that add flavor to our food also face quite a few challenges before landing on our plate. One such challenge is the virulent fungus Colletotrichum truncatum, which causes infections in various plants, and the anthracnose disease in chillies (Capsicum annuum). In chillies, the disease is identified with sunken abrasion as concentric rings and rotting of the chilli fruit. The disease results in the loss of yield for chilli farmers. For a country that produced 1492.10 thousand tonnes of chillies in 2014-15, or 36 % of global production, yielding Rs. 4000 crores to the economy, the anthracnose infection in chillies poses a serious threat to its economy.

“The disease has been reported to cause up to 50% losses in chilli yield in India with 8-27% loss reported in Maharashtra, 20-60% in Punjab and Haryana, and 30 – 76 % in Tamil Nadu”, points out Dr. Madhusudhan Reddy Nandineni, Staff Scientist at the Centre for DNA Fingerprinting and Diagnostics (CDFD), Hyderabad. In a recent study, he and his student Ms. Soumya Rao have sequenced the genome of C. truncatum. Their work, published in the journal PLoS ONE, aids in better understanding of the pathogen and helps in devising a scheme for controlling its spread. The researchers studied the fungal genes that secretes enzymes that degrade cell wall (secretory protease), proteins that suppress plant defense response (effectors) and pathogenic agents -- secondary metabolites (SM) that are responsible for virulent nature of the fungus.

So how does Colletotrichum truncatum attack chilli plants? The researchers found that the fungus first secretes carbohydrate metabolizing enzymes like glycoside hydrolases, carbohydrate esterases, polysaccharide lyases, and others. These enzymes degrade the host’s cell wall components like chitin, cellulose, hemicellulose, pectin, etc. and thus the fungus colonizes the host cell. The secretory proteases secreted by the fungus such as metalloprotease, serine proteases, fungalysin and cysteine protease prevent the fungus from being attacked by the host’s immune system and facilitates its entry. Upon entry into host cell, the secondary metabolites produced by the fungus helps in starting up the infection.

The host plant, on its side, tries to defend itself by producing antimicrobial compounds, secondary metabolites and toxins as defense mechanism. But the fungus destroys them by enzymatic degradation. The researchers have identified specific genes, transporters and transcription factors in the fungus that might enable in exporting the toxins and host antimicrobial compounds. They are believed to help in nutrient uptake as well. The effector proteins of the fungus modify the host’s genes and takes control of the host system. The carbohydrate active enzymes of the fungus are believed to be the causative agent for rotting of the fruit by destroying the outer thick cuticle and cell walls of the chilli fruit.

The study also compares the genomes of C. truncatum with other Colletotrichum species and has decoded the proteins in its genome. It found that C. truncatum possess few unique genes, and also shares many with other species of Colletotrichum genus. 13,724 genes of the fungus were studied and were found to have ~ 89% similarity with other Colletotrichum species. Decoding the pathogenic genes paves way for understanding the process of the infection and spread of the disease.

The study is a major step in understanding the physiology of one of the causative agents for reducing crop yields. Many such studies are needed to help tackle the problem of diseases in the food we grow. “Similar studies in C. truncatum would help in understanding the mechanism of infection and discovery of novel strategies to control anthracnose in field”, signs off Dr. Nandineni.

So, when next time you try to throw a chilli from your plate, salute it as it is one among the survivor which manifested its purpose of life -- adding spice to your food.