A Newly Evolved Gene Blocks Reproduction Between Two Nematode Species by Destroying a Key Protein

What is it about?

The identification of speciation genes and how they interact to form reproductive barriers are long-standing mysteries. In this study, we demonstrate how a newly evolved gene in one species of free-living soil worms, Caenorhabditis nigoni, prevents successful reproduction of C. nigoni with its close relative, C. briggsae. The gene, called Cni-neib-1, is involved in protein degradation and only targets an essential protein in C. briggsae, but not in C. nigoni, causing the hybrid embryos to die during development. This process effectively prevents the two species from interbreeding and mixing their genetic material. The research reveals a previously unknown mechanism of the two-gene incompatibility, offering a new explanation for how reproductive barriers form and evolve.

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Photo by Uriel Soberanes on Unsplash

Photo by Uriel Soberanes on Unsplash

Why is it important?

This research is important because it provides a detailed example of how the Dobzhansky-Muller model of hybrid incompatibility operates at the molecular level, which is rarely documented. The Dobzhansky-Muller model explains how reproductive barriers can arise when genes from two different species negatively interact in hybrids. In this study, we identify the precise components involved: a newly evolved F-box gene, Cni-neib-1, from C. nigoni, and a conserved gene Cbr-shls-1 from C. briggsae. Their interaction leads to the degradation of an essential protein in hybrid embryos, resulting in their death. This is significant because it shows, for the first time, how a simple two-gene interaction can directly cause hybrid incompatibility through protein degradation. Additionally, the study highlights the critical role of protein degradation and immune response in this process. F-box genes, like Cni-neib-1, are often responsible for targeting proteins for destruction, and their rapid evolution may be driven by the need to adapt to species-specific immune challenges. This suggests that the expansion of F-box genes in C. nigoni may be an evolutionary response to environmental pressures, but with unintended consequences in hybrids. By linking protein degradation to reproductive isolation, this research offers new insights into the mechanisms of speciation and emphasizes the potential role of immune-related genes in driving species divergence.