About

Abby Dernburg, PhD, is the Principal Investigator of the Dernburg Lab at the University of California, Berkeley. She holds a PhD from the University of California, San Francisco, and a B.A. in Biochemistry from the University of California, Berkeley. The lab's webpage lists her as the lead faculty member, indicating her role in directing research and mentoring a diverse team including postdoctoral scholars, graduate students, and interns. Contact information is provided as afdernburg(at)berkeley.edu. The page primarily serves as a team directory and does not provide detailed descriptions of her specific research focus or key scientific contributions.

Research topics

• Evolutionary biology
• Computational biology
• Genetics
• Biology

Selected publications

• NPP-21/TPR is required for developmental control of spindle checkpoint strength in <i>C. elegans</i>

  bioRxiv (Cold Spring Harbor Laboratory) · 2026-04-15

  articleOpen access

  Abstract The spindle checkpoint ensures accurate chromosome segregation by monitoring whether chromosomes, via kinetochores, are properly attached to the spindle. If chromosomes fail to establish bipolar attachment, the checkpoint delays the cell cycle to enable error correction. In C. elegans early embryos, activation of the spindle checkpoint produces a longer mitotic delay in primordial germ cells than somatic cells. We show that the conserved nucleoporin and spindle matrix component, NPP-21/TPR, is required for the stronger spindle checkpoint in germline cells. A checkpoint-proficient NPP-21::GFP transgene localizes to a spindle-like structure during mitosis and is enriched in germline cells, consistent with a cell-fate specific function for this protein. Finally, NPP-21 controls spindle checkpoint strength in germline cells via two, potentially linked, mechanisms: concentrating PCH-2 around mitotic chromosomes and promoting the localization of the checkpoint effector, Mad2, to unattached kinetochores. These experiments demonstrate a developmental role for NPP-21, and the spindle matrix, in controlling spindle checkpoint strength in immortal germline cells in C. elegans .

  PublisherOA PDFDOI

• Dynamic molecular architecture of the synaptonemal complex

  Science Advances · 2025-01-22 · 15 citations

  articleOpen accessSenior authorCorresponding

  During meiosis, pairing between homologous chromosomes is stabilized by the assembly of the synaptonemal complex (SC). The SC ensures the formation of crossovers between homologous chromosomes and regulates their distribution. However, how the SC regulates crossover formation remains elusive. We isolated an unusual mutation in Caenorhabditis elegans that disrupts crossover interference but not SC assembly. This mutation alters the unique C terminal domain of an essential SC protein, SYP-4, a likely ortholog of the vertebrate SC protein SIX6OS1. We use three-dimensional stochastic optical reconstruction microscopy (3D-STORM) to interrogate the molecular architecture of the SC from wild-type and mutant C. elegans animals. Using a probabilistic mapping approach to analyze super-resolution image data, we detect changes in the organization of the synaptonemal complex in wild-type animals that coincide with crossover designation. We also found that our syp-4 mutant perturbs SC architecture. Our findings add to growing evidence that the SC is an active material whose molecular organization contributes to chromosome-wide crossover regulation.

  PublisherDOI

• Crossover patterning through condensation and coarsening of pro-crossover factors

  Nature Cell Biology · 2025-06-19 · 14 citations

  articleOpen accessSenior author
  PublisherOA PDFDOI

• Chemically induced proximity reveals a Piezo-dependent meiotic checkpoint at the oocyte nuclear envelope

  Science · 2024-11-21 · 15 citations

  articleSenior authorCorresponding

  Sexual reproduction relies on robust quality control during meiosis. Assembly of the synaptonemal complex between homologous chromosomes (synapsis) regulates meiotic recombination and is crucial for accurate chromosome segregation in most eukaryotes. Synapsis defects can trigger cell cycle delays and, in some cases, apoptosis. We developed and deployed a chemically induced proximity system to identify key elements of this quality control pathway in Caenorhabditis elegans . Persistence of the polo-like kinase PLK-2 at pairing centers—specialized chromosome regions that interact with the nuclear envelope—induced apoptosis of oocytes in response to phosphorylation and destabilization of the nuclear lamina. Unexpectedly, the Piezo1/PEZO-1 channel localized to the nuclear envelope and was required to transduce this signal to promote apoptosis in maturing oocytes.

  PublisherDOI

• How to build the virtual cell with artificial intelligence: Priorities and opportunities

  Cell · 2024-12-01 · 258 citations

  articleOpen access

  Cells are essential to understanding health and disease, yet traditional models fall short of modeling and simulating their function and behavior. Advances in AI and omics offer groundbreaking opportunities to create an AI virtual cell (AIVC), a multi-scale, multi-modal large-neural-network-based model that can represent and simulate the behavior of molecules, cells, and tissues across diverse states. This Perspective provides a vision on their design and how collaborative efforts to build AIVCs will transform biological research by allowing high-fidelity simulations, accelerating discoveries, and guiding experimental studies, offering new opportunities for understanding cellular functions and fostering interdisciplinary collaborations in open science.

  PublisherDOI

• ATM signaling modulates cohesin behavior in meiotic prophase and proliferating cells

  Nature Structural & Molecular Biology · 2023-03-06 · 20 citations

  articleOpen accessSenior author

  Cohesins are ancient and ubiquitous regulators of chromosome architecture and function, but their diverse roles and regulation remain poorly understood. During meiosis, chromosomes are reorganized as linear arrays of chromatin loops around a cohesin axis. This unique organization underlies homolog pairing, synapsis, double-stranded break induction, and recombination. We report that axis assembly in Caenorhabditis elegans is promoted by DNA-damage response (DDR) kinases that are activated at meiotic entry, even in the absence of DNA breaks. Downregulation of the cohesin-destabilizing factor WAPL-1 by ATM-1 promotes axis association of cohesins containing the meiotic kleisins COH-3 and COH-4. ECO-1 and PDS-5 also contribute to stabilizing axis-associated meiotic cohesins. Further, our data suggest that cohesin-enriched domains that promote DNA repair in mammalian cells also depend on WAPL inhibition by ATM. Thus, DDR and Wapl seem to play conserved roles in cohesin regulation in meiotic prophase and proliferating cells.

  PublisherDOI

• MJL-1 is a nuclear envelope protein required for homologous chromosome pairing and regulation of synapsis during meiosis in <i>C. elegans</i>

  Science Advances · 2023-02-08 · 10 citations

  articleOpen accessSenior authorCorresponding

  Interactions between chromosomes and LINC (linker of nucleoskeleton and cytoskeleton) complexes in the nuclear envelope (NE) promote homolog pairing and synapsis during meiosis. By tethering chromosomes to cytoskeletal motors, these connections lead to processive chromosome movements along the NE. This activity is usually mediated by telomeres, but in the nematode Caenorhabditis elegans , special chromosome regions called “pairing centers” (PCs) have acquired this meiotic function. Here, we identify a previously uncharacterized meiosis-specific NE protein, MJL-1 (MAJIN-Like-1), that is essential for interactions between PCs and LINC complexes in C. elegans . Mutations in MJL-1 eliminate active chromosome movements during meiosis, resulting in nonhomologous synapsis and impaired homolog pairing. Fission yeast and mice also require NE proteins to connect chromosomes to LINC complexes. Extensive similarities in the molecular architecture of meiotic chromosome-NE attachments across eukaryotes suggest a common origin and/or functions of this architecture during meiosis.

  PublisherOA PDFDOI

• A cooperative network at the nuclear envelope counteracts LINC-mediated forces during oogenesis in <i>C. elegans</i>

  Science Advances · 2023-07-12 · 7 citations

  articleOpen accessSenior authorCorresponding

  , oocyte nuclei lacking the single lamin protein LMN-1 are vulnerable to collapse under forces mediated through LINC (linker of nucleoskeleton and cytoskeleton) complexes. Here, we use cytological analysis and in vivo imaging to investigate the balance of forces that drive this collapse and protect oocyte nuclei. We also use a mechano-node-pore sensing device to directly measure the effect of genetic mutations on oocyte nuclear stiffness. We find that nuclear collapse is not a consequence of apoptosis. It is promoted by dynein, which induces polarization of a LINC complex composed of Sad1 and UNC-84 homology 1 (SUN-1) and ZYGote defective 12 (ZYG-12). Lamins contribute to oocyte nuclear stiffness and cooperate with other inner nuclear membrane proteins to distribute LINC complexes and protect nuclei from collapse. We speculate that a similar network may protect oocyte integrity during extended oocyte arrest in mammals.

  PublisherOA PDFDOI

• Author response: Recruitment of Polo-like kinase couples synapsis to meiotic progression via inactivation of CHK-2

  2023-01-17

  peer-reviewOpen accessSenior author

  Most animals, plants, and fungi reproduce sexually, meaning that the genetic information from two parents combines during fertilization to produce offspring. This parental genetic information is carried within the reproductive cells in the form of chromosomes. Reproductive cells in the ovaries or testes first multiply through normal cell division, but then go through a unique type of cell division called meiosis. During meiosis, pairs of chromosomes – the two copies inherited from each parent – must find each other and physically line up from one end to the other. As they align side-by-side with their partners, chromosomes also go through a mixing process called recombination, during which regions of one chromosome cross over to the paired chromosome to exchange information. Scientists are still working to understand how this process of chromosome alignment and crossing-over is controlled. If chromosomes fail to line up or cross over during meiosis, eggs or sperm can end up with too many or too few chromosomes. If these faulty reproductive cells combine during fertilization this can lead to birth defects and developmental problems. To minimize this problem, reproductive cells have a quality control mechanism during meiosis called “crossover assurance”, which limits how often mistakes occur. Zhang et al. have investigated how cells can tell if their chromosomes have accomplished this as they undergo meiosis. They looked at egg cells of the roundworm C. elegans, whose meiotic processes are similar to those in humans. In C. elegans, a protein called CHK-2 regulates many of the early events during meiosis. During successful meiosis, CHK-2 is active for only a short amount of time. But if there are problems during recombination, CHK-2 stays active for longer and prevents the cell division from proceeding. Zhang et al. uncovered another protein that affects for how long CHK-2 stays switched on. When chromosomes align with their partners, a protein called PLK-2 sticks to other proteins at the interface between the aligned chromosomes. A combination of microscopy and test tube experiments showed that when PLK-2 is bound to this specific location, it can turn off CHK-2. However, if the chromosome alignment fails, PLK-2 is not activated to switch off CHK-2. Therefore, CHK-2 is only switched off when the chromosomes are properly aligned and move on to the next step in crossing-over, which then allows meiosis to proceed. Thus, PLK-2 and CHK-2 work together to detect errors and to slow down meiosis if necessary. Further experiments in mammalian reproductive cells will reveal how similar the crossover assurance mechanism is in different organisms. In the future, improved understanding of quality control during meiosis may eventually lead to improvements in assisted reproduction.

  PublisherDOI

• Chemically induced proximity reveals mechanotransduction of a meiotic checkpoint at the nuclear envelope

  bioRxiv (Cold Spring Harbor Laboratory) · 2023-10-28 · 2 citations

  preprintOpen accessSenior authorCorresponding

  Abstract Successful sexual reproduction relies on robust quality control during meiosis. Assembly of the synaptonemal complex between homologous chromosomes (synapsis) regulates meiotic recombination and is crucial for accurate chromosome segregation in most eukaryotes. Synapsis defects can trigger cell cycle delays and, in some cases, apoptosis. Here, by developing and deploying a new chemically induced proximity system, we iden-tify key players in this quality control pathway in Caenorhabditis elegans . We find that persistence of the Polo-like kinase PLK-2 at pairing centers, specialized chromosome regions that interact with the nuclear envelope to promote homolog pairing and synapsis, induces apoptosis of oocytes by phosphorylating and destabilizing the nuclear lamina. Unexpectedly, we find that a mechanosensitive Piezo1/PEZO-1 channel localizes to the nuclear envelope and is required to transduce this signal to promote apoptosis. Thus, mechanosensitive ion channels play essential roles in detecting nuclear events and triggering apoptosis during gamete production. One-sentence summary Destabilization of the nuclear lamina triggers Piezo-dependent germline apoptosis.

  PublisherOA PDFDOI

Recent grants

• Crossover control during meiosis

  NIH · $4.5M · 2002–2021

Frequent coauthors

• Liangyu Zhang

  Fujian Medical University

  169 shared

• Simone Köhler

  European Molecular Biology Laboratory

  93 shared

• Zhouliang Yu

  Yunnan University

  76 shared

• Chenshu Liu

  University of California, Los Angeles

  71 shared

• Julie Ahringer

  University of Cambridge

  66 shared

• Ofer Rog

  University of Utah

  58 shared

• Ericca Stamper

  56 shared

• Regina Rillo-Bohn

  Howard Hughes Medical Institute

  48 shared

Labs

• Dernburg LabPI

  The Dernburg Lab studies the mechanisms of cell division and the role of the cytoskeleton in cell shape and movement.

Education

• Postdoctoral , Developmental Biology

  Stanford University School of Medicine

  2000

• Ph.D., Biochemistry and Biophysics

  University of California, San Francisco

  1996

• B.A., Biochemistry

  University of California, Berkeley

  1987