CAPRIN1 specifically mediates m6A modification of RIG-I RNA to inhibit Mycobacterium Tuberculosis infection.

Tuberculosis (TB), the leading cause of death from a single infectious agent, remains incompletely understood in its pathogenic mechanisms. Through population-based bioinformatic analyses, we identified m6A modifications may play a critical role in the infection dynamics of tuberculosis, with CAPRIN1 emerging as a TB-specific m6A regulatory factor. Molecular and cellular experiments demonstrated that CAPRIN1 regulates the m6A modification of RIG-I RNA through direct interaction with METTL3, further influencing downstream interferon-associated gene networks and modulating Mycobacterium tuberculosis (M. tuberculosis) infection. Moreover, we discovered that these molecular biological processes predominantly occur within cellular stress granules (SGs). In summary, this study elucidates a CAPRIN1-specific m6A modification mechanism targeting RIG-I, proposing a potential target for the prevention and treatment of TB. and contributing to the theory of m6A's specific regulatory roles.