P. pacificus’s epigenetic toolkit is missing an important tool

Epigenetics has the potential to help us understand key differences in how divergent species control gene expression. Recent work published by Brown et al. in GENETICS delves into the epigenetic mechanisms of Pristionchus pacificus, providing significant insights into the evolutionary dynamics of epigenetic regulation.

Many developmental traits are sensitive to environmental factors, and the differences in how close evolutionary relatives respond to their environments can help demystify development. The nematode Pristionchus pacificus has been established as a comparative system to the well-studied Caenorhabditis elegans, but a thorough exploration of the conservation of epigenetic pathways between the two species has not been conducted—until now.

P. pacificus is known for its remarkable morphological plasticity, especially in its feeding structures. It appears to be a perfect model to study the epigenetic regulation of these adaptive changes; however, its relative newness as a model system means its epigenetic “toolkit” isn’t well-defined. To manipulate the proteins and modifications involved in the epigenetics of plasticity, they first must be identified.

To address this gap, Brown et al. began with an in-silico approach to identify potential epigenetic genes, followed by biochemical analysis to identify histone posttranslational modifications. By orthology, they then predicted which proteins might be responsible for adding or removing these marks. Their work provides a comprehensive “epigenetic toolkit” for P. pacificus and reveals significant differences in epigenetic machinery between P. pacificus and C. elegans, highlighting the evolutionary flexibility of epigenetic regulation and underscoring the importance of understanding species-specific epigenetic landscapes.

One of the authors’ most striking findings is that P. pacificus lacks the repressive PRC2 complex, which is usually crucial for histone methylation. Surprisingly, the enzymatic product H3K27me3 is still present, suggesting an unknown methyltransferase is responsible for this modification. The revelation that P. pacificus can maintain a critical histone modification while missing its canonical enzyme opens the door to myriad new paths of investigation.

This work serves as a foundational resource for future studies on developmental plasticity and epigenetic regulation in P. pacificus. It also provides a comparative framework for studying similar mechanisms in other species, offering new avenues for research in evolutionary biology and epigenetics.