UW Genome Sciences

 

Wednesdays, 3:30, Foege Auditorium (Foege S-060) unless otherwise noted | remote viewing option

UW Genome Sciences brings leading researchers from a broad spectrum of scientific areas to campus to discuss the latest advances in genetics, genomics, proteomics, computational research and related emerging tools and technologies.

subscribe or unsubscribe to the email list | past seminars

Not all seminars are recorded, but those which are will be posted to the past seminars page and deleted after two weeks. Please note that a current UW NetID is required to access past seminar recordings.

Winter 2026

2/25

3/4

3/11 - Dr. Taro Kitazawa | Aarhus University
"Whole-genome single-cell history-tracing to reveal neuronal identity transition and memory formation"
talk will not be recorded

Memory defines who we are. Converging studies propose that memories are allocated to a sparse ensemble of neurons that are activated during learning and reactivated during recall. However, only a limited fraction of learning-activated neurons is reactivated, and the cellular and molecular mechanisms that determine reactivation propensity remain unknown.
In the first half of this seminar, I will focus on memory allocation during learning and present our single-cell (sc) multi-omics approach. After aversive memory formation, we collected the amygdala, medial prefrontal cortex, and dorsal hippocampus and performed 10x Genomics scMultiome (RNA and ATAC) together with multimodal nanobody-scCUT&Tag (nanoCT; ATAC plus H3K27ac, H3K27me3, and FOS). By focusing on the epigenetic memory of neuronal activation, we identified learning-specific gene regulatory modules distinct from baseline activity, outlining regulatory programs by which neurons discriminate learning-relevant stimuli (manuscript in preparation).
In the second half, I will introduce HisTrac-seq, a whole-genome history-tracing platform we developed to overcome the snapshot limitation of conventional single-cell sequencing. HisTrac-seq enzymatically labels adenines in genomic DNA to record past gene regulatory states, enabling “time machine”-like temporal multi-omics that links past and present molecular profiles within the same cells. We extended HisTrac-seq to single cells and, in a neurodifferentiation dataset, discovered unexpected abrupt cell identity transitions (“identity jumps”) associated with alterations in signaling and epigenetic states (Kawamura et al., bioRxiv 2025).
Finally, I will introduce our ongoing scHisTrac-seq study of memory, which links learning-induced molecular states to recall-time reactivation. This enables a direct comparison of reactivated versus non-reactivated neurons to uncover the epigenetic and transcriptional basis of ensemble reactivation - a core feature of the memory engram definition.

Whole-genome single-cell multimodal history tracing to reveal cell identity transition. Kawamura, KY., Khalil, V., Kitazawa, T. bioRxiv 2025 (https://doi.org/10.1101/2025.08.12.669973)

Spring 2026

4/1 - Dr. Huaiying Zhang | Carnegie Mellon University
"Formation and Function of Chromatin-Associated Condensates"
talk will not be recorded

4/8 - Dr. Steven McCarroll | Harvard University

4/15 - Dr. Andrew Murray | Harvard University
"Beyond DraftKings: Yeast cells also hedge their bets"
talk will be recorded

Microorganisms live in unpredictable and rapidly changing environments. Bet-hedging is one way for a population to deal with this volatility: even though they share the same genome, different cells can use different strategies. In brewer’s yeast, we name the two strategies arrestors and recoverers: arrestors grow faster than recoverers on high glucose concentrations but fail to recover and restart growth when they must metabolize a worse carbon source, like ethanol, whereas recoverers eventually restart their growth and division. The two phenotypes result from the bistability of a dynamical system and are epigenetically heritable with switches from one to another occurring every few cell divisions. The heart of bistability is a competition between cytoplasmic and mitochondrial protein synthesis. Most mitochondrial proteins, including the protein components of the mitochondrial ribosome, are encoded in the nuclear genome and translated in the cytoplasm before being imported into the mitochondria. In contrast, the greasiest components of the electron transport chain are encoded in the mitochondrial DNA and are made by mitochondrial ribosomes. In recoverers, the charge difference across the mitochondrial inner membrane is high, they import the proteins of the mitochondrial ribosome, the ribosomes they form translate the mitochondrially encoded components of the electron transport chain, and the cells both respire and ferment glucose. In contrast, the charge difference across the mitochondrial inner membrane of arrestors is small, they fail to import the proteins of the mitochondrial ribosome, they cannot translate the mitochondrially encoded components of the electron transport chain and they can only ferment glucose. The steady state fractions of arrestors and recoverers are under genetic and environmental control and we can demonstrate this bistability as far as fission yeast, which last shared a common ancestor with budding yeast 500 million years ago.

 

4/22 - reserved

4/29 - no seminar

Thursday, 4/30, 1:00 - Dr. Mark Kokoris | Roche
sponsored jointly with UW Bioengineering

5/6 - Dr. Richard Sever | openRxiv

5/13 - Dr. Koseki Kobayashi | University of Chicago

5/20

5/27 - no seminar

6/3 - Dr. Pablo Cardenas | Cornell University

Autumn 2026

10/28 - Dr. Jonathan Pritchard | Stanford University

11/4 - Dr. Hernan Garcia | UC Berkeley