About

Neil Hunter is a Principal Investigator at the Hunter Lab within the Department of Microbiology and Molecular Genetics at UC Davis. The webpage lists him as a key member of the research team, indicating his role in leading scientific investigations in this field. The lab's focus includes microbiology and molecular genetics, although specific details about his research interests, background, or key contributions are not provided on the page. The site also features a team of research specialists, graduate students, postdoctoral scholars, and research technicians working under his direction, emphasizing his leadership role in a collaborative research environment.

Research topics

• Biology
• Cell biology
• Genetics
• Medicine
• Internal medicine
• Surgery

Selected publications

• Polycomb shapes active chromatin and promoter bivalency during ovarian reserve formation and activation

  bioRxiv (Cold Spring Harbor Laboratory) · 2026-04-25

  articleOpen access

  The ovarian reserve, a finite pool of long-lived non-growing oocytes established at birth, determines female reproductive lifespan, yet how these oocytes establish long-term quiescence while retaining the capacity for future growth and embryogenesis remains poorly understood. Here, we define a regulatory logic by which Polycomb repressive complexes shape stage-specific active chromatin remodeling during ovarian reserve formation and early oocyte growth. During ovarian reserve formation, H3K27ac, an active promoter- and enhancer-associated mark, undergoes extensive genome-wide redistribution. A key feature of this transition is CpG island promoter remodeling, in which many loci lose H3K27ac while gaining PRC1-dependent H2AK119ub, a repressive mark. This early reprogramming is followed during oocyte growth by acquisition of PRC2-dependent H3K27me3, de novo establishment of bivalent promoters, and protection of promoter regions from de novo DNA methylation. Oocyte growth is also accompanied by broad gains in both H3K27ac and H3K4me3, an active promoter-associated mark. Analyses of PRC1- and PRC2-deficient oocytes reveal unequal Polycomb contributions: PRC2 broadly constrains H3K27ac, whereas PRC1 more selectively shapes genome-wide H3K27ac redistribution and restricts H3K4me3 accumulation at bivalent promoters. Together, these findings identify staged active chromatin remodeling as an integral feature of perinatal oocyte development and reveal that Polycomb shapes chromatin state transitions as oocytes enter quiescence and become poised for future growth.

  PublisherOA PDFDOI

• SUMO mediates the coordinate regulation of meiotic chromosome length and crossover rate

  bioRxiv (Cold Spring Harbor Laboratory) · 2026-03-11

  articleOpen accessSenior authorCorresponding

  SUMMARY Meiotic prophase-I chromosomes are organized into linear arrays of chromatin loops anchored to proteinaceous axes that define the interaction interfaces for the pairing and synapsis of homologous chromosomes. Chromatin loop size and axial chromosome length are inversely correlated and vary widely both between and within species, including between the sexes. The molecular basis of this variation remains unclear. Here, we provide evidence that the small ubiquitin-like modifier, SUMO, regulates loop–axis organization in mouse meiosis. Our analysis shows that the longer axes of oocyte chromosomes contain more SUMO per unit length than the shorter axes of spermatocyte chromosomes. In mouse models, the loss of SUMO1 results in shorter axes and longer chromatin loops. Conversely, increased SUMO1 conjugation, caused by mutation of the SENP1 isopeptidase, produces longer axes with shorter loops. Axis length positively correlates with meiotic recombination. Accordingly, Sumo1 and Senp1 mutations respectively decrease and increase crossover frequency. These findings identify SUMO as a key regulator of meiotic chromosome architecture and suggest a molecular basis for the physiological variation in chromosome length and recombination rates seen among species, sexes, individuals, and individual meiocytes. GRAPHICAL ABSTRACT

  PublisherOA PDFDOI

• Polycomb Repressive Complex 1 primes non-growing oocytes for growth and early embryogenesis

  Cell Research · 2026-02-23

  articleOpen access
  PublisherOA PDFDOI

• SUMO modulates meiotic crossover rates between and within vertebrate species

  bioRxiv (Cold Spring Harbor Laboratory) · 2026-03-27

  articleOpen access

  Abstract Crossing over during meiosis drives genetic diversity and ensures the accurate segregation of homologous chromosomes. Variation in the rate of crossing over has been linked to evolutionary divergence and environmental adaptability, shaping fitness and responses to selective pressures. Despite its significance, the molecular mechanisms underlying this variation remain poorly understood. Crossover sites are selected from a large pool of potential sites initiated by programmed DNA double-strand breaks. Post-translational modification by SUMO (Small Ubiquitin-like Modifier) has been implicated in this process. Here, we show that crossover rate, chromosome length, and abundance of chromosome-associated SUMO are positively correlated across a range of vertebrate species, including mouse, chicken, pig, cattle, sheep, and goat. Crossover variation between goat breeds across the Indian subcontinent was also positively correlated with chromosomal SUMO level. Furthermore, modulating SUMO levels in cultured goat spermatocytes altered crossover frequency. Cumulatively, these observations point to a central role for SUMO in mediating crossover variation both between and within vertebrate species.

  PublisherOA PDFDOI

• Distinct and interdependent functions of three RING proteins regulate recombination during mammalian meiosis

  Proceedings of the National Academy of Sciences · 2025-01-06 · 12 citations

  articleOpen accessSenior authorCorresponding

  During meiosis, each pair of homologous chromosomes becomes connected by at least one crossover, as required for accurate segregation, and adjacent crossovers are widely separated thereby limiting total numbers. In coarsening models, this crossover patterning results from nascent recombination sites competing to accrue a limiting pro-crossover RING-domain protein (COR) that diffuses between synapsed chromosomes. Here, we delineate the localization dynamics of three mammalian CORs in the mouse and determine their interdependencies. RNF212, HEI10, and the newest member RNF212B show divergent spatiotemporal dynamics along synapsed chromosomes, including profound differences in spermatocytes and oocytes, that are not easily reconciled by elementary coarsening models. Contrasting mutant phenotypes and genetic requirements indicate that RNF212B, RNF212, and HEI10 play distinct but interdependent functions in regulating meiotic recombination and coordinating the events of meiotic prophase-I by integrating signals from DNA breaks, homolog synapsis, the cell-cycle, and incipient crossover sites.

  PublisherOA PDFDOI

• HEIP1 orchestrates pro-crossover protein activity during mammalian meiosis

  Proceedings of the National Academy of Sciences · 2025-10-21 · 2 citations

  articleOpen access

  Meiotic crossovers (COs) are needed to produce genetically balanced gametes. In mammals, CO formation is mediated by a conserved set of pro-CO proteins via mechanisms that remain unclear. Here, we characterize a mammalian pro-CO factor HEIP1. In mouse HEIP1 is essential for crossover and fertility of both sexes. HEIP1 promotes crossover by orchestrating the recruitment of other pro-CO proteins, including the MutSγ complex (MSH4-MSH5) and E3 ligases (HEI10, RNF212, and RNF212B), that are required to mature CO sites and recruit the CO-specific resolution complex MutLγ. Moreover, HEIP1 directly interacts with HEI10, suggesting a direct role in controlling the recruitment of pro-CO E3 ligases. During early stages of meiotic prophase I, HEIP1 interacts with the chromosome axes, independently of recombination, before relocalizing to the central region of the synaptonemal complex. We propose that HEIP1 is a conserved master regulator of CO proteins that controls different CO maturation steps.

  PublisherOA PDFDOI

• Primary human ovarian interstitial cells contribute to murine follicle growth through follicle-interstitial paracrine crosstalk

  Research Square · 2025-09-24

  preprintOpen access
  PublisherOA PDFDOI

• Protecting double Holliday junctions ensures crossing over during meiosis

  Nature · 2025-09-24 · 10 citations

  articleOpen accessSenior authorCorresponding

  Abstract Chromosomal linkages formed through crossover recombination are essential for the accurate segregation of homologous chromosomes during meiosis 1 . The DNA events of recombination are linked to structural components of meiotic chromosomes 2 . Imperatively, the biased resolution of double Holliday junction (dHJ) intermediates into crossovers 3,4 occurs within the synaptonemal complex (SC), the meiosis-specific structure that mediates end-to-end synapsis of homologues during the pachytene stage 5,6 . However, the role of the SC in crossover-specific dHJ resolution remains unclear. Here we show that key SC components function through dependent and interdependent relationships to protect dHJs from aberrant dissolution into non-crossover products. Conditional ablation experiments reveal that cohesin, the core of SC lateral elements, is required to maintain both synapsis and dHJ-associated crossover recombination complexes (CRCs) during pachytene. The SC central region transverse-filament protein is also required to maintain CRCs. Reciprocally, the stability of the SC central region requires the continuous presence of CRCs effectively coupling synapsis to dHJ formation and desynapsis to resolution. However, dHJ protection and CRC maintenance can occur without end-to-end homologue synapsis mediated by the central element of the SC central region. We conclude that local ensembles of SC components are sufficient to enable crossover-specific dHJ resolution to ensure the linkage and segregation of homologous chromosomes.

  PublisherOA PDFDOI

• An Epigenomic Roadmap Primes Non-Growing Oocytes for Maturation and Early Embryogenesis

  SSRN Electronic Journal · 2025-01-01 · 1 citations

  preprintOpen access
  PublisherDOI

• SPO11 cuts!

  Cell Research · 2025-03-16

  articleOpen accessSenior author
  PublisherOA PDFDOI

Recent grants

• Meiosis, SUMOylation and the ZIP3 Protein: Parallel Studies in Mouse and Yeast.

  NIH · $1.2M · 2009–2015

• Joint Molecule Resolution During Meiotic Recombination

  NIH · $6.0M · 2005–2026

Frequent coauthors

• Walter Lisch

  Saarland University

  3192 shared

• Berthold Seitz

  Saarland University

  3173 shared

• Andreas Janecke

  Innsbruck Medical University

  3173 shared

• Alexander K. C. Leung

  863 shared

• Alexander K. C. Leung

  694 shared

• Peter L. M. Jansen

  University of Arizona

  680 shared

• Michael Trauner

  Medical University of Vienna

  507 shared

• Lee A. Denson

  501 shared

Labs

• Hunter LabPI

Education

• Postdoctoral Fellow, Genetics, Molecular and Cellular Biology

  Harvard University

  2002

• PhD Genetics, Weatherall Institute of Molecular Medicine

  University of Oxford

  1996

• BSc Biochemistry and Applied Molecular Biology

  University of Manchester

  1992

Awards & honors

• Fellow of The Royal Society (2025)
• Microbiology Excellence in Undergraduate Research (2018)