Fungal Genome Defense: TRISS Links Two Ancient Systems to Silence Jumping Genes During Sex

What is it about?

All living things—from humans to fungi—have "junk" DNA, like viruses and transposons (or "jumping genes"), that can disrupt their normal genes and threaten the stability of their genomes. Organisms evolve defense systems to fight these genetic parasites, especially during sexual reproduction when two genomes combine. We discovered a brand-new fungal defense mechanism, which we call TRISS (Tandem Repeat-Induced Sexual Silencing), in the important plant pathogen Fusarium graminearum. TRISS is like a specialized immune system that becomes active only during the fungus's sexual stage. Unlike other known fungal defenses, TRISS is uniquely triggered by repeated sequences of DNA and uses a specialized form of RNA interference (RNAi). The most remarkable finding is that TRISS acts as a bridge, linking the two most famous fungal defenses: the DNA-mutating system called RIP and the RNA-based silencing system. This link allows the fungus to silence genetic threats at both the DNA (genetic) and protein-production (post-transcriptional) levels simultaneously, ensuring these harmful elements aren't passed to the next generation. This strategy is highly effective and helps maintain the fungus's unusually clean, repeat-poor genome.

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Photo by digitale.de on Unsplash

Photo by digitale.de on Unsplash

Why is it important?

Our work is unique and timely for several reasons: 1. The First Known RIP-RNAi Link: For nearly 40 years, the fungal defense system Repeat-Induced Point mutation (RIP) has been studied as a DNA-level mutation mechanism, while RNA interference (RNAi) has been studied separately. We are the first to demonstrate that the RIP key protein, Rid, is required for a new RNAi pathway, TRISS, to function. This discovery reveals a conserved, integrated strategy where two ancient genome defense systems work together for maximal protection during sexual reproduction. 2. Novel Mechanism of Action: TRISS siRNAs (called trasiRNAs) are perfectly complementary to their targets but primarily cause translational repression (stopping protein production) instead of the typical mRNA destruction (slicing). This highlights a rare, underappreciated mechanism for genome defense. 3. Rethinking RNAi Amplification: We show that TRISS amplifies its silencing signal not through the classical "transitive RNAi" chain reaction, but through a direct protein-recruitment feedback loop. Key proteins (Sms2 and Rid) interact with a universal DNA-binding protein (RPA) to quickly and efficiently summon the core RNAi machinery to the site of the genetic threat. The Difference It Might Make： 1. Fundamental Biology Insight: This study fundamentally changes our understanding of how eukaryotic genomes defend themselves, particularly during sexual development. The integrated RIP-RNAi mechanism may be a conserved strategy across many filamentous fungi. 2. Pathogen Control: F. graminearum is a major crop pathogen causing Fusarium Head Blight. By dissecting TRISS, we provide a potential new target for chemical intervention to destabilize the fungus's genome defense, making it more susceptible to external factors or genetic manipulation, which is critical for developing new control strategies. 3. New Perspective on RIP: Our findings give new molecular clues into the long-standing mystery of how the RIP C-to-T mutations occur, by showing that the RIP mediator Rid interacts with RPA, a protein that can protect DNA repair intermediates.

Perspectives