Jia-Xing Yue (岳家兴)

@iamphioxus.bsky.social

PI of @EvomicsLab.bsky.social (www.evomicslab.org) at Sun Yat-sen University Cancer Center Editor of @genomebiolevol.bsky.social and @yeast-journal.bsky.social Alumni of @cnrs.fr @ircan.bsky.social @RiceUniversity @NanjingUniversity

An attempt to explain what this does, using a simple case. How much 'tangle' in a synteny plot comes how we chose to order chromosomes, and how much is unavoidable because it represents accurate crossings in the data? 1/

a tangled synteny plot with 55 crossings on the left, and its solved partner on the right with only 9 crossings
Joe Hanly@hanliconius.bsky.social · 6d ago

I've complained on here a few times about synteny plots that are harder to read than they need to be. I decided it was time to actaully do something about it: introducing SynTangle, a tool for untangling whole-genome synteny plots github.com/Hanliconius/... 1/

How long does DNA damage last? @aaronquinlan.bsky.social and I found evidence that lesions are transmitted from parent (P0) to offspring (F1) in C. elegans. If they segregate unrepaired for multiple cell divisions, lesions generate multi-allelism in the F1 germline. www.biorxiv.org/content/10.6...

Inherited DNA damage generates multi-allelic mutations in C. elegans

Exogenous and endogenous mutagens generate a wide variety of DNA lesions, including bulky adducts, chemical modifications, and single- or double-stranded breaks. A phenomenon called “lesion segregation,” in which lesions evade repair and persist for multiple cell divisions, has recently been documented in tumors and healthy somatic tissues from mice and humans, respectively. Persistent lesions can generate multi-allelic variants (MAVs) by serving as templates for multiple rounds of error-prone replication. By reanalyzing data from a large C. elegans mutagenesis experiment, we observed robust evidence for MAVs at a small fraction (∼0.2%) of mutated sites in the offspring of strains treated with alkylating agents. Because these sequencing data were derived from the progeny of a single F1 animal — itself the offspring of a mutagenized P0 — all mutations should be biallelic. The presence of multi-allelic variation implies that some DNA lesions are transmitted to the F1 zygote, evade repair, and are repeatedly bypassed by error-prone polymerases during embryogenesis. We suspect that many more lesions are inherited than is suggested by MAV prevalence, and that a large fraction of biallelic mutations are also caused by inherited lesions. Our results demonstrate that DNA lesions serve as durable, transgenerational templates for mutagenesis in C. elegans . We speculate that lesion segregation in the early embryo may be a source of mosaicism and genetic diversity in humans, as well. ### Competing Interest Statement The authors have declared no competing interest. National Institutes of Health, https://ror.org/01cwqze88, R01HG012252

biorxiv.org

Great collaboration with Dr. Na Liu and Dr. Jun Ma's teams! It was a fun journey to expand our research footprint into cancer-associated microorganisms. Special thanks to @simonemozzachiodi.bsky.social for critically reading our manuscript and providing valuable feedback. 🧬🦠

Evomics Lab@evomicslab.bsky.social · 3mo ago

Glad to see this joint work on nasopharyngeal microbiota culturomics published in #ScienceTranslationalMedicine, featured as a cover story! By building this local bacterial catalog, we characterized a Fusobacterium-Prevotella mutualism in nasopharyngeal tumors. www.science.org/doi/10.1126/...

How good is MiniBWA, the successor to BWA? To test it, I ran MiniBWA on sequencing from 76 different species, comparing mapping speed, rate and accuracy with BWA MEM. In short, it's really good. If you map short reads, it's well worth your time. andrewcarroll.github.io/2026/06/30/t...

The Best of Both Worlds - Assessing MiniBWA

Recently, Heng Li released MiniBWA (GitHub) alongside a paper by Heng Li and Nils Homer describing the method (paper). MiniBWA builds on the approaches in Minimap2 (also by Heng Li), but falls back on...

andrewcarroll.github.io

Such a big relief to see my much belated PhD project finally wrapped up, after so many years and so much ups and downs ... "It is a long way from amphioxus, but we all came from there" ~

Evomics Lab@evomicslab.bsky.social · 7mo ago

Excited to share our PNAS paper on the genome evolution of an early-diverging #amphioxus, Asymmetron lucayanum! There is a long and twisty story behind this work, which also explains the username choice of the lab PI @iamphioxus.bsky.social . 😀 @pnas.org www.pnas.org/doi/10.1073/...

very happy to have this work published in mbe @molbioevol.bsky.social can now use phyloHessian to get a (hopefully) improved div time & subs rate estimate, particularly for deep-time or fast‑evolving lineages github.com/evolbeginner... #julialang #iqtree #mcmctree #molecularclock

GitHub - evolbeginner/phyloHessianWrapper

Contribute to evolbeginner/phyloHessianWrapper development by creating an account on GitHub.

github.com

Molecular Biology and Evolution@molbioevol.bsky.social · 8mo ago

@sishuowang.bsky.social & Meade introduce phyloHessian, using complex mixture substitution models in molecular dating. Empirical analysis of ancient symbiont lineages leads to a revised understanding of their host association origins. 🔗 doi.org/10.1093/molbev/msag039 #evobio #molbio #compbio