Michael Lampson · University of Pennsylvania · PhdFit
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Michael Lampson
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University of Pennsylvania · Rehabilitation Medicine
Michael Lampson is an Assistant Professor of Biology at the University of Pennsylvania, affiliated with the Department of Biology and the Cell and Molecular Biology graduate group. His research focuses on the mechanisms of cell division, particularly the interactions between chromosomes and spindle microtubules, and the regulation of these processes by mitotic kinases. He investigates how kinetochore-microtubule interactions are controlled to ensure accurate chromosome segregation and maintain genome integrity, utilizing experimental approaches such as chemically-induced dimerization, FRET-based biosensors, and photoactivatable fluorescent proteins. Additionally, Lampson studies chromosome evolution through biased segregation in meiosis, known as meiotic drive, exploring how non-Mendelian segregation influences karyotype evolution and speciation. His work employs mouse models and advanced cell biological techniques to elucidate the mechanisms underlying meiotic drive and chromosome segregation, providing insights into fundamental cell biology and evolutionary processes.
Journal of the American Chemical Society · 2026-02-09
articleOpen accessCorresponding
Traditional pharmacology has limited control of drug activity and localization in space and time. Herein, we describe an approach for kinase regulation using conditional localization pharmacology (CLP), where an inactive caged inhibitor is localized to a site of interest in a dormant state using intracellular protein tethering. The activity of the inhibitor can be regulated with spatial and temporal precision in a live cellular environment using light. As a proof of concept, a photocaged MPS1 kinase inhibitor (reversine) bearing a HaloTag ligand tether was designed to manipulate the cell cycle. We demonstrate that this new caged reversine halo probe (CRH) strategy is capable of efficient localization and exceptional spatiotemporal control over spindle assembly checkpoint (SAC) silencing and mitotic exit.
bioRxiv (Cold Spring Harbor Laboratory) · 2026-05-18
articleSenior author
Summary Long-read sequencing has enabled precise measurements of highly repetitive centromeric satellites and their rapid divergence between species 1–7 . Large satellite arrays emerge from libraries of shorter arrays via stochastic expansions 8,9 , but understanding the selective pressures constraining such expansions remains a major challenge. Here, using the mouse “major” satellite as a model, we reveal reciprocal functional constraints between increasing satellite copy number and abundance of a conserved architectural protein in female meiosis. We show that HMGA2 (high mobility group AT-hook 2) is enriched at major satellite, and its expression correlates with major satellite copy number: both are high in Mus musculus compared to the closely related Mus spretus . To test functional constraints, we modulated HMGA2 abundance by depletion or overexpression and used a musculus / spretus hybrid to generate oocytes with intermediate HMGA2 expression and major satellite copy number. We find that HMGA2 depletion disrupts major satellite packaging in major satellite-rich musculus but not hybrid oocytes, indicating that increasing copy number requires high HMGA2 expression. Conversely, HMGA2 overexpression disrupts chromosome segregation in major satellite-poor spretus but not hybrid oocytes, indicating that high HMGA2 expression requires expanded major satellite arrays. Based on these results, we propose a co-evolution model in which satellite expansion is constrained by architectural protein abundance, whereas protein abundance is constrained reciprocally by satellite array size.
Current Opinion in Genetics & Development · 2025-07-15 · 1 citations
reviewOpen accessSenior authorCorresponding
Centromeres are essential for genome inheritance, serving as sites for kinetochore assembly and for final sister chromatid cohesion to ensure accurate chromosome segregation during cell division. These roles must persist through radical physical changes to chromosomes and other biological challenges presented by specialized processes in the germlines of both sexes and during early embryonic development. Centromeres in most organisms are epigenetically defined by the presence of a histone H3 variant, CENP-A. Therefore, to maintain centromeres, CENP-A nucleosomes must be inherited across generations through the germline. However, unique aspects of gametogenesis, including asymmetric meiosis and prolonged cell cycle arrest in the female germline and extensive chromatin reorganization in the male germline, introduce additional layers of complexity to the process of centromere inheritance. Here, we review the implications of these processes for centromere regulation during gametogenesis and early embryonic development, drawing on findings from mouse and fruit fly models.
bioRxiv (Cold Spring Harbor Laboratory) · 2025-01-29 · 2 citations
preprintOpen accessSenior authorCorresponding
Telomere length is inherited directly as a DNA sequence and as a classic quantitative trait controlled by many genes across the genome. Here, we show that neither paradigm fully accounts for telomere length inheritance, which also depends on a parent-of-origin effect on telomere elongation in the early embryo. By reciprocally crossing mouse strains with different telomere lengths, we find that telomeres elongate in hybrid embryos only when maternal telomeres are short and paternal telomeres are long. In the reciprocal cross, telomeres shorten. These differences in embryonic telomere elongation, which emerge before zygotic genome activation, predict adult telomere length. Moreover, when telomeres do elongate, we find molecular signatures of a recombination-based mechanism of telomere elongation, called the Alternative Lengthening of Telomeres (ALT) pathway, previously suggested to elongate telomeres in the pre-implantation embryo. We propose that ALT is triggered by a combination of genetic asymmetry in telomere length and epigenetic asymmetry between maternal and paternal chromosomes in the zygote. Our findings offer new insight into the complex interaction of genetic and epigenetic determinants of telomere length inheritance.
Genome Biology and Evolution · 2025-02-01 · 3 citations
articleOpen access
A species tree is a central concept in evolutionary biology whereby a single branching phylogeny reflects relationships among species. However, the phylogenies of different genomic regions often differ from the species tree. Although tree discordance is widespread in phylogenomic studies, we still lack a clear understanding of how variation in phylogenetic patterns is shaped by genome biology or the extent to which discordance may compromise comparative studies. We characterized patterns of phylogenomic discordance across the murine rodents-a large and ecologically diverse group that gave rise to the laboratory mouse and rat model systems. Combining recently published linked-read genome assemblies for seven murine species with other available rodent genomes, we first used ultraconserved elements (UCEs) to infer a robust time-calibrated species tree. We then used whole genomes to examine finer-scale patterns of discordance across ∼12 million years of divergence. We found that proximate chromosomal regions tended to have more similar phylogenetic histories. There was no clear relationship between local tree similarity and recombination rates in house mice, but we did observe a correlation between recombination rates and average similarity to the species tree. We also detected a strong influence of linked selection whereby purifying selection at UCEs led to appreciably less discordance. Finally, we show that assuming a single species tree can result in substantial deviation from the results with gene trees when testing for positive selection under different models. Collectively, our results highlight the complex relationship between phylogenetic inference and genome biology and underscore how failure to account for this complexity can mislead comparative genomic studies.
bioRxiv (Cold Spring Harbor Laboratory) · 2024-10-13 · 1 citations
preprintOpen accessSenior authorCorresponding
Abstract Pericentromeres are heterochromatic regions adjacent to centromeres that ensure accurate chromosome segregation. Despite their conserved function, they are composed of rapidly evolving A/T-rich satellite DNA. This paradoxical observation is partially resolved by epigenetic mechanisms that maintain H3K9me3-based heterochromatin, independent of specific DNA sequences. However, these mechanisms can function only after H3K9me3 has already been established, and this mark is absent from paternal chromatin in the mouse zygote. It is unknown how variation in satellite DNA sequence impacts alternative forms of heterochromatin at this earliest stage of life. Here we show functional consequences of satellite DNA variation for pericentric heterochromatin formation, recruitment of the Chromosome Passenger Complex (CPC), and interactions with the mitotic spindle. The AT-hook of Polycomb Repressive Complex 1 (PRC1) directly recognizes A/T-rich satellite DNA and packages it in H2AK119ub1 heterochromatin. By fertilizing M. musculus eggs with sperm from other mouse species, we show that divergent satellite sequences differ in their ability to bind PRC1, resulting in differences in H2AK119ub1 heterochromatin formation on mitotic chromosomes. Furthermore, we find that satellites that robustly form H2AK119ub1 inhibit molecular pathways that recruit the CPC to pericentromeres, increasing microtubule forces on kinetochores during mitosis. Our results provide a direct link between satellite DNA composition and pericentromere function and highlight early embryogenesis as a critical point in development that is sensitive to satellite DNA evolution.
