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Layton, E. M.

Publications and source records attributed to Layton, E. M..

2 recordsLinked to original sources

The phage stress test: a proving ground for genome language models in biological prediction

Reliable biological prediction by AI is most likely to emerge first in the simplest systems with rich datasets and the fastest opportunities for testing and refinement. Phages with small genomes are an ideal testbed. Decades of experimental work have created an unusually information-rich literature benchmark that sits largely outside the sequence repositories typically used to train genome language models (GLMs). Recent work has shown that GLMs such as Evo2 can generate viable whole bacteriophage genomes, demonstrating that genome-scale biological design is possible. The next question is more mechanistic: can such models correctly predict the effects of simple, local sequence changes? Here, we evaluated Evo2 against experimental mutation data from two model phages: the single-stranded RNA phage MS2 and the single-stranded DNA phage {Phi}X174. We first addressed whether Evo2 sequence log-likelihood scores could distinguish viable from nonviable mutations, and then whether models trained on Evo2 embeddings were predictive of function. Across both phages, Evo2 captured expected sequence-level constraints: stop codons were generally penalized, synonymous substitutions had higher likelihood than nonsynonymous substitutions. Evo2 distinguished among synonymous codons in ways only weakly explained by host codon usage. However, for MS2, these capabilities did not translate into robust biological predictions. Specifically, Evo2 {Delta}SLL failed to distinguish functional from nonfunctional mutations in the lysis gene, an overlapping viral region that appears to be a particularly hard test case. In {Phi}X174, performance was stronger but still modest, and much of the apparent signal could be explained by simple covariates such as nonsense mutations, genomic position, and nucleotide distance from the reference. Together, these results introduce phages as a tractable proving ground for stress-testing GLMs against experimentally grounded genotype-to-phenotype tasks. More broadly, they provide a durable framework for identifying what data and model ingredients are required for biologically reliable prediction.

bioinformatics↗

A single prophage WO gene rescues cytoplasmic incompatibility in Drosophila melanogaster

Wolbachia are maternally-inherited, intracellular bacteria at the forefront of vector control efforts to curb arbovirus transmission. In international field trials, the cytoplasmic incompatibility (CI) drive system of wMel Wolbachia is deployed to replace target vector populations, whereby a Wolbachia- induced modification of the sperm genome kills embryos. However, Wolbachia in the embryo rescue the sperm genome impairment, and therefore CI results in a strong fitness advantage for infected females that transmit the bacteria to offspring. The two genes responsible for the wMel-induced sperm modification of CI, cifA and cifB, were recently identified in the eukaryotic association module of prophage WO, but the genetic basis of rescue is unresolved. Here we use transgenic and cytological approaches to demonstrate that cifA independently rescues CI and nullifies embryonic death caused by wMel Wolbachia in Drosophila melanogaster. Discovery of cifA as the rescue gene and previously one of two CI induction genes establishes a new Two-by-One model that underpins the genetic basis of CI. Results highlight the central role of prophage WO in shaping Wolbachia phenotypes that are significant to arthropod evolution and vector control.\n\nSignificance StatementThe World Health Organization recommended pilot deployment of Wolbachia-infected mosquitoes to curb viral transmission to humans. Releases of mosquitoes are underway worldwide because Wolbachia can block replication of these pathogenic viruses and deterministically spread by a drive system termed cytoplasmic incompatibility (CI). Despite extensive research, the underlying genetic basis of CI remains only half-solved. We recently reported that two prophage WO genes recapitulate the modification component of CI in a released strain for vector control. Here we show that one of these genes underpins rescue of CI. Together, our results reveal the complete genetic basis of this selfish trait and pave the way for future studies exploring WO prophage genes as adjuncts or alternatives to current control efforts.

genetics↗