Biology subjects

Koreshova, A.

Publications and source records attributed to Koreshova, A..

5 recordsLinked to original sources

bioRxiv2026

Conflicts and coalitions among selfish toxin-antidote elements shape the evolution of hyperdivergent haplotypes

Genetic conflict drives evolutionary innovation, yet most research has focused on arms races between selfish elements and their hosts. A second layer-competition among selfish elements-remains largely unexplored. Here, we uncover such a conflict between two antagonistic toxin-antidote elements (TAs), loki-1/sgyn-1 and thor-1/sif-1, in Caenorhabditis tropicalis. Each toxin, LOKI-1 or THOR-1, selectively kills progeny homozygous for the opposing haplotype, favoring heterozygotes. Their antidotes, SGYN-1 and SIF-1, evolved from F-box proteins, although SIF-1 subsequently lost its F-box domain. We solved the crystal structure of the THOR-1-SIF-1 complex and used in vivo mutagenesis to validate the binding interface, supporting direct toxin neutralization independently of F-box-mediated degradation. A survey of 676 wild isolates revealed two contrasting evolutionary outcomes of antagonizing TAs: independently evolved loki-1/sgyn-1 and thor-1/sif-1 remain confined to alternative hyperdivergent haplotypes, whereas other homologous TAs can recombine to form composite haplotypes. Altogether, our findings establish competition among selfish elements as a distinct form of genetic conflict, and support models in which antagonistic TAs act as barriers that restrict gene flow between neighboring populations.

evolutionary biology↗

bioRxiv2024

A regulatory module driving the recurrent evolution of irreducible molecular complexes.

To sustain life, molecular complexes require the concerted action of multiple proteins, each relying on one another to perform intricate tasks. However, how such interdependent protein interactions evolve in the first place is poorly understood. To address this, we investigated the origins of a group of fast-evolving genetic parasites--toxin-antidote elements--which boil down this dilemma to a simple question: what came first, the toxin or the antidote? By integrating quantitative genetics, biochemistry, and evolutionary genomics, we discovered that toxins and antidotes can arise simultaneously through the duplication of a regulatory module comprising an F-box protein in linkage to its substrate. Our findings provide one solution to the recurrent emergence of mutual dependence in protein complexes and illustrate in detail how complexity can swiftly arise from simplicity.

genomics↗

bioRxiv2022

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↗

bioRxiv2022

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↗

bioRxiv2020

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↗