Tyler Kent

@tylervkent.bsky.social

Postdoc @ University of Chicago Ecology & Evolution Evolutionary genomics mostly The opinions expressed are my own, and they do not necessarily represent the views or opinions of my employer

🚨 The Grieshop Lab is hiring at all levels!!! 🚨 Oct 2027 start: 👉 4-year BBSRC-funded PhD position (closes 30 Nov) 👉 3.5-year NERC-funded PhD position (closes 16 Dec) Feb 2027 start: 👉 3-year NERC-funded post-doc 👉 3-year NERC-funded lab tech 👉 (part-time) 3-year NERC-funded tech

Just over two weeks left to apply! I may be biased, but it’s hard to imagine a better place to do plant evolutionary biology.

Jeffrey Ross-Ibarra@jrossibarra.bsky.social · 2mo ago

I am excited to announce a job for an Asst Prof in Plant Evolution in the dept. of Evolution and Ecology at @ucdavis.bsky.social. We're looking broadly, from macro (speciation, comparative genomics, evo-devo) to micro (pop biology, adaptive evolution, evo-eco). recruit.ucdavis.edu/JPF07777

New preprint with grad student @linhngk.bsky.social. Big mystery in plants is why do their telomere length vary? We answered by analyzing 10Tb or 1.4 billion reads from 257 species of algae to land plants. We propose ecological adaptation shapes telomere length in plants. shorturl.at/0ox4x

Biogeographic cline is associated with the global plant telomere length variation

Telomeres have the crucial role of protecting chromosome ends and its length varies significantly between organisms. What evolutionary factor shapes this natural variation has been a long standing que...

biorxiv.org

Exciting news: @uwgenome.bsky.social will be hiring for two tenure-track faculty positions this year, one open rank and one assistant professor. Both are “Genome Sciences” interpreted broadly so we welcome applicants working in a variety of fields and methods. Ad will be out shortly.

The (literal) closing of a chapter, former Schrider Lab student Amjad Dabi's paper where he simulates evolutionary rescue scenarios to model the dynamics of treatment resistance in sequential cancer therapy is now published in PLoS Comp Bio: journals.plos.org/ploscompbiol... (1/5)

Evolutionary rescue model informs strategies for driving cancer cell populations to extinction

Author summary Cancer cells often evolve resistance to treatments during therapy by acquiring specific mutations, leading to eventual relapse and treatment failure. While using multiple treatments in ...

journals.plos.org

Dan Schrider@samurscicop.bsky.social · 2y ago

In the latest from the lab (www.biorxiv.org/content/10.1...), PhD student Amjad Dabi used simulation to investigate the emergence of resistance to therapy in cancer under an evolutionary rescue model. Why does treatment for some cancers fail after a period of initial effectiveness? (1/n)

New preprint! 🎉 How do populations adapt to a changing environment? We show how standing genetic variation enables polygenic adaptation, while the speed and magnitude of environmental change can determine whether populations adapt—or go extinct. www.biorxiv.org/content/10.6...

Standing genetic variation drives polygenic adaptation to different environmental shifts

Most organisms are well adapted to the environment they have been exposed to for many generations. However, changing environments pose existential threats to populations, unless they are able to adapt...

biorxiv.org

If anyone looking for a postdoc with fantastic genomics/bioinformatics skills + strong intellect + great energy, please let me know! Preferably West Coast or remote/hybrid options & the candidate is open to a short (1 year) or longer term appointment

"...solving problems is only a tool and proxy for achieving the primary goal of conceptual understanding and insight. Forgetting this in the world of AI may turn the tool against the primary goal."

Terence Tao@teorth.bsky.social · last mo.

A group of 25 Fields Medalists, including myself, have made a joint declaration on Math and AI: mathandai.org . We welcome additional signatories. See also this article in the Economist announcing the declaration: www.economist.com/science-and-...

I’m looking to hire an NIH funded postdoc to join our lab here at Davis (please RT). Ongoing areas of interest include: 1) polygenic signals of selection from time series, ARGs, GWAS, etc 2) The interpretation of GWAS, polygenic scores, & sources of confounding

Our lab's first journal cover! Art by @taylorblack.bsky.social and project led by @brynnjohnson13.bsky.social

Taylor Black@taylorblack.bsky.social · last mo.

SO PROUD! @brynnjohnson13.bsky.social’s paper on temp dependent competition in secondary contact zones in darters is ofFISHally out in @journal-evo.bsky.social academic.oup.com/evolut/artic... As an extra hurrah related to this work, I had the opportunity to paint a corresponding journal cover!

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