RACK-1, a multifaceted regulator is required for C. elegans innate immunity against S. flexneri M9OT infection.

The nematode C. elegans has the ability to clear off bacterial colonization in the intestine using pathogen specific innate immune response. Here, we show that C. elegans RACK-1 has been vital in determining the survival of worms under specific pathogenic infection. Among various pathogens tested, S. flexneri M9OT (SF) exhibited highest pathogenicity by killing rack-1 mutant worm-VC3013 earlier when compared to WT. The expression level of rack-1 mRNA was found to be decreased and it further indicated that the host translational event appeared to be affected during SF infection. Hence, inhibition of translational machinery was the foremost reason for the early mortality in C. elegans. Apparently, variation in the expression of RACK-1 affects the activation of p38 and JNK-MAPK pathway which consequently triggered expression of nlp-29 and longevity, respectively. The study unveils novel defense mechanisms exist for C. elegans in facilitating enhanced immunity by RACK-1 against SF infection.

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