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Widen, S. A.

Publications and source records attributed to Widen, S. A..

3 recordsLinked to original sources

Virus-like transposons cross the species barrier and drive the evolution of genetic incompatibilities

Horizontal gene transfer--the movement of genetic material between different species--has been reported across all major eukaryotic lineages, including vertebrates. However, the underlying mechanisms of transfer and their impact on genome evolution are still poorly understood. While studying the evolutionary origin of a selfish element in the nematode C. briggsae, we discovered that Mavericks, ancient viral-like transposons related to giant viruses and virophages, are one of the long-sought vectors of horizontal gene transfer. We found that Mavericks gained a novel herpesvirus-like fusogen in nematodes, leading to the widespread exchange of cargo genes between extremely divergent species, bypassing sexual and genetic barriers spanning hundreds of millions of years. Our results show how the union between viruses and transposons--natures melting pot--causes horizontal gene transfer and ultimately genetic incompatibilities in natural populations.

genomics↗

The evolution of an RNA-based memory of self in the face of genomic conflict

Distinguishing endogenous genes from selfish ones is essential for germline integrity. In animals, small regulatory RNAs play a central role in this process; however, the underlying principles are largely unknown. To fill this gap, we studied how selfish toxin-antidote elements (TAs) evade silencing in the nematode Caenorhabditis tropicalis. We found that the slow-1/grow-1 TA is active only when maternally inherited. Surprisingly, this parent-of-origin effect stems from a regulatory role of the toxins mRNA: maternal slow-1 mRNA--but not SLOW-1 protein--licenses slow-1 expression in the zygote by counteracting piRNAs. Our results indicate that epigenetic licensing-- known to play a role in C. elegans sex-determination--is likely a common mechanism that hinders the spread of selfish genes in wild populations while ensuring a lasting memory of self in the germline.

genetics↗

Ubiquitous selfish toxin-antidote elements in Caenorhabditis species

Toxin-antidote elements (TAs) are selfish genetic dyads that spread in populations by selectively killing non-carriers. TAs are common in prokaryotes, but few examples are known in animals. We discovered five maternal-effect TAs in the nematode Caenorhabditis tropicalis and one in C. briggsae. Unlike previously reported TAs, five of these novel toxins do not kill embryos but instead cause larval arrest or developmental delay. We identified the genes underlying a TA causing developmental delay, slow-1/grow-1, and found that the toxin, slow-1, is homologous to nuclear hormone receptors. Last, we found that balancing selection of conflicting TAs hampers their ability to drive in populations, leading to more stable genetic incompatibilities. Our results show that TAs are common in Caenorhabditis species, target a wide range of developmental processes, and may act as barriers preventing gene flow.

genomics↗