About

Professor Kerry Bloom leads the Bloom Lab, which is dedicated to uncovering the fundamental biophysical and molecular principles governing genome organization, chromosomal mechanics, and nuclear architecture. The lab emphasizes understanding how mechanical forces, structural transitions, and spatial organization contribute to genome stability and cellular function. Their research focuses on centromere biology and chromosome fragility, particularly under mechanical stress and genomic perturbation, as well as kinetochore and spindle mechanics, exploring how force and chromatin structure contribute to chromosome segregation. Additionally, the lab investigates pericentromeric and nucleolar compartmentalization, including the role of DNA-protein and RNA-mediated phase separation, and the polymer physics of chromatin, studying how transient crosslinking and chromatin network properties drive nuclear organization and condensate formation. These studies integrate live-cell imaging, molecular genetics, and statistical physics modeling to reveal chromatin as a responsive and mechanically active material in space and time. Professor Bloom's research redefines genome regulation as a dynamic physical system responsive to force, topology, and emergent material properties rather than merely a biochemical code. Insights from the lab explain how cells maintain genomic stability under stress, why certain genome regions such as centromeres and rDNA are hotspots for fragility and repair, and how nuclear architecture adapts during development, disease, and evolution. The lab's work also elucidates fundamental mechanisms behind diseases like cancer, where chromosomal instability and altered nuclear mechanics are critical. By integrating molecular cell biology with polymer physics and systems modeling, Professor Bloom contributes to a paradigm shift in conceptualizing the genome as matter governed by the laws of physics rather than solely information.

Research topics

• Genetics
• Cell biology
• Biology
• Molecular biology
• Biophysics
• Computational biology

Selected publications

• Coordinated chromosome motion emerges from mechanical coupling mediated by the physical spindle environment

  bioRxiv (Cold Spring Harbor Laboratory) · 2026-01-20

  articleOpen access

  Abstract During metaphase, chromosomes undergo oscillatory motion and exhibit distance-dependent coordinated movement with neighboring chromosomes within the spindle. However, the physical mechanism that gives rise to coordinated chromosome motion remains unclear. Here, we combine quantitative live-cell imaging in PTK1 cells, targeted perturbations of spindle microtubules and chromatin, and minimal mechanical modeling to uncover the mechanical basis of chromosome coordination during metaphase. We show that chromosome oscillations are dampened by stabilizing microtubules or by decondensing chromatin, yet inter-chromosomal coordination is preserved. The dissociation between chromosome oscillations and chromosome coordination suggests that coordination can arise from forces transmitted through the spindle environment. To test this idea, we developed a minimal mechanical model in which oscillating chromosome pairs are coupled through transient inter-chromosomal springs, while oscillations of each chromosome pair are generated by feedback between kinetochore-microtubule dynamics and centromere elasticity. The model demonstrates that stochastic mechanical connections are sufficient to generate correlated chromosome motion. To quantify chromosome coordination in a manner that reflects the mechanical properties of the surrounding spindle environment, we employed a microrheology-inspired analysis of time-lagged chromosome displacements. This framework reveals that microtubules and chromatin play distinct mechanical roles: microtubules primarily determine the spatial range and temporal build-up of coordination, while chromatin tunes its strength. Together, our results establish coordinated chromosome motion as an emergent mechanical property of the mitotic spindle, mediated by its viscoelastic properties and collective force transmission.

  PublisherOA PDFDOI

• eLife Assessment: Enhanced Processivity and Collective Force Production of Kinesin-1 at Low Radial Forces

  2026-01-13

  peer-reviewOpen access1st authorCorresponding

  Kinesin-1 is a robust motor that carries intracellular cargos towards the plus ends of microtubules. However, optical trapping studies reported that kinesin-1 is a slippery motor that quickly detaches from the microtubule, and multiple kinesins are incapable of teaming up to generate large collective forces. This may be due to the vertical (z) forces that the motor experiences in a single bead trapping assay, accelerating the detachment of the motor from a microtubule. Here, we substantially lowered the z-force by using a long DNA handle between the motor and the trapped bead and characterized the motility and force generation of single and multiple kinesin-1s. Contrary to previous views, we show that kinesin-1 is a robust motor that resists microtubule detachment before it reaches high hindering forces, but it quickly detaches under assisting forces even at low z-forces. We also demonstrate highly efficient collective force generation by multiple kinesin-1 motors. These results provide an explanation for how multiple kinesins team up to perform cellular functions that require higher forces than a single motor can bear.

  PublisherDOI

• eLife Assessment: DNA tensiometer reveals catch-bond detachment kinetics of kinesin-1, -2 and -3

  2026-03-26

  peer-reviewOpen access1st authorCorresponding

  Bidirectional cargo transport by kinesin and dynein is essential for cell viability and defects are linked to neurodegenerative diseases. Computational modeling suggests that the load-dependent off-rate is the strongest determinant of which motor ‘wins’ a kinesin-dynein tug-of-war, and optical tweezer experiments find family-dependent differences in the sensitivity of detachment to load, with kinesin-3 > kinesin-2 > kinesin-1. However, in reconstituted kinesin-dynein pairs vitro, all three kinesin families compete nearly equally well against dynein. Modeling and experiments have confirmed that vertical forces inherent to the large trapping beads enhance kinesin-1 dissociation rates. In vivo, vertical forces are expected to range from negligible to dominant, depending on cargo and microtubule geometries. To investigate the detachment and reattachment kinetics of kinesin-1, 2 and 3 motors against loads oriented parallel to the microtubule, we created a DNA tensiometer comprising a DNA entropic spring attached to the microtubule on one end and a motor on the other. Kinesin dissociation rates at stall were slower than detachment rates during unloaded runs, and the complex reattachment kinetics were consistent with a weakly-bound ‘slip’ state preceding detachment. Kinesin-3 behaviors under load suggested that long KIF1A run lengths result from the concatenation of multiple short runs connected by diffusive episodes. Stochastic simulations were able to recapitulate the load-dependent detachment and reattachment kinetics for all three motors and provide direct comparison of key transition rates between families. These results provide insight into how kinesin-1, -2 and -3 families transport cargo in complex cellular geometries and compete against dynein during bidirectional transport.

  PublisherDOI

• Different relative scalings between transient forces and thermal fluctuations tune regimes of dynamic clustering.

  UNC Libraries · 2026-04-28

  articleOpen access1st authorCorresponding

  An example system of collective behavior in the presence of active agents is the structural maintenance of chromosome (SMC) protein complexes within the nucleus that create an architecture to facilitate the organization and proper function of the genome. Of the diverse functions these SMC proteins are capable of producing, we focus on the creation of localized clusters of chromatin in the nucleolus through transient cross-links. Large-scale simulations revealed three different dynamic behaviors as a function of timescale: slow cross-linking leads to no clusters, fast cross-linking produces rigid slowly changing clusters, while intermediate timescales produce flexible clusters that mediate gene interaction. By mathematically analyzing different relative scalings of the two sources of stochasticity, thermal fluctuations, and the force induced by the transient cross-links, we predict these three distinct regimes of cluster behavior. Standard time averaging that takes the fluctuations of the transient cross-link force to zero predicts the existence of rigid clusters. Accounting for the interaction of both fluctuations from the cross-links and thermal noise with an effective energy landscape predicts the timescale-dependent lifetimes of flexible clusters. No clusters are predicted when the fluctuations of the transient cross-link force are taken to be large relative to thermal fluctuations. This mathematical perturbation analysis illuminates the importance of accounting for stochasticity in local incoherent transient forces to predict emergent complex biological behavior.

  PublisherDOI

• Coordinated chromosome motion emerges from mechanical coupling mediated by the physical spindle environment

  Molecular Biology of the Cell · 2026-04-29

  articleSenior author

  During metaphase, chromosomes undergo oscillatory motion and exhibit distance-dependent coordinated movement with neighboring chromosomes within the spindle. However, the physical mechanism that gives rise to coordinated chromosome motion remains unresolved. Here, we combine quantitative live-cell imaging in PTK1 cells, targeted perturbations of spindle microtubules and chromatin condensation level, and minimal mechanical modeling to uncover the mechanical basis of chromosome coordination during metaphase. We show that chromosome oscillations are dampened by stabilizing microtubules or by reducing chromatin condensation, yet inter-chromosomal coordination measured by Pearson's correlation coefficient is preserved across all conditions. Consistently, simulations show that Pearson's correlation is insensitive to the mechanical parameters governing inter-chromosomal coupling. Together, these observations motivate the hypothesis that chromosome coordination is a mechanical signature of the physical spindle environment. To test this hypothesis, we developed a minimal mechanical model incorporating transient inter-chromosomal springs as a general representation of inter-chromosomal interactions, and show they are sufficient to generate correlated chromosome motion. To quantify coordination in a manner that reflects the mechanical properties of the surrounding spindle environment, we employed a microrheology-inspired analysis of time-lagged chromosome displacements applied to both experimental and simulated data, revealing that microtubules set the spatial range of coordination while chromatin condensation level modulates its strength. Together, our results support the hypothesis that coordinated chromosome motion is an emergent mechanical property of the mitotic spindle.

  PublisherDOI

• HP1-enhanced chromatin compaction stabilizes a synthetic metabolic circuit in yeast

  bioRxiv (Cold Spring Harbor Laboratory) · 2025-03-06

  preprintOpen access

  Abstract Chromatin compaction defines genome topology, evolution, and function. The Saccharomycotina subphylum, including the fermenting yeast Saccharomyces cerevisiae have a decompacted genome, possibly because they lost two genes mediating a specific histone lysine methylation and histone binding protein heterochromatin protein 1 (HP1). This decompaction may result in the higher-than-expected mutation and meiotic recombination rates observed in this species. To test this hypothesis, we retro-engineered S. cerevisiae to compact the genome by expressing the HP1 homologue of Schizosaccharomyces pombe Sp Swi6 and H3K9 methyltransferase Sp Clr4. The resulting strain had significantly more compact chromatin and reduced rates of mutation and meiotic recombination. The increased genomic stability significantly prolongs the optogenetic control of an engineered strain designed to grow only in blue light. This result demonstrates the potential of our approach to enhance the stability of strains for metabolic engineering and other synthetic biology applications, which are prone to lose activities due to genetic instability.

  PublisherDOI

• eLife Assessment: Enhanced Processivity and Collective Force Production of Kinesins at Low Radial Forces

  2025-11-07

  peer-reviewOpen access1st authorCorresponding

  Kinesin-1 is a robust motor that carries intracellular cargos towards the plus ends of microtubules. However, optical trapping studies reported that kinesin-1 is a slippery motor that quickly detaches from the microtubule, and multiple kinesins are incapable of teaming up to generate large collective forces. This may be due to the vertical (z) forces that the motor experiences in a single bead trapping assay, accelerating the detachment of the motor from a microtubule. Here, we substantially lowered the z-force by using a long DNA handle between the motor and the trapped bead and characterized the motility and force generation of single and multiple kinesin-1s. Contrary to previous views, we show that kinesin-1 is a robust motor that resists microtubule detachment before it reaches high hindering loads, but it quickly detaches under assisting loads even at low z-forces. We also demonstrate highly efficient collective force generation by multiple kinesin-1 motors. These results provide an explanation for how multiple kinesins team up to perform cellular functions that require higher forces than a single motor can bear.

  PublisherDOI

• Tuning nuclear rheology through transient chromatin cross-links

  Physical review. E · 2025-11-17 · 1 citations

  articleOpen access

  In eukaryotic cells, the nucleolus is a pivotal subnuclear organelle, instrumental in ribosomal RNA synthesis and nuclear organization. Although the unique viscoelastic properties of the nucleolus are associated with transient interactions between chromatin and regulatory proteins, the specific mechanistic details driving nucleolar phase separation and mechanical responses have remained largely undefined. In this study, we employ a computational approach to elucidate chromatin-protein interactions within the nucleolus of budding yeast, using a sophisticated bead-spring polymer model. This model integrates DNA and nucleolar architectures with dynamic simulations of interactions involving chromosomal structural maintenance proteins and rDNA transcriptional regulators through systematically varied cross-linking kinetics. Our findings reveal that modulations in protein-DNA interactions critically dictate the phase behavior, relaxation dynamics, and viscoelastic properties of the nucleolus, underscoring a complex but precise regulatory mechanism at play. Notably, protein-mediated bridging emerges as a critical factor enhancing nucleolar condensation and modulating stress relaxation, highlighting the transformative role of transient cross-linking in nuclear mechanics regulation. These insights not only deepen our understanding of nucleolar function but also open avenues for interventions in genetic engineering and disease therapeutics.

  PublisherOA PDFDOI

• The Role of Transient Crosslinks in the Chromatin Search Response to DNA Damage

  UNC Libraries · 2025-12-12

  articleOpen access

  Homology search is a means through which DNA double-strand breaks (DSBs) explore the genome for sequences that enable error-free repair, known as homologous recombination. A better understanding of this search process is fundamental to the relationship between higher-order chromosome organization and DNA damage. Here, we use an entropic bead-spring polymer chain model to simulate the spatiotemporal dynamics of the yeast genome during interphase. The chromosome is organized by transient and dynamic cross-links representing structural maintenance of chromosome (SMC) complexes. DNA damage is modeled as a break in the bead-spring chain, coupled with a removal of crosslinks from beads proximal to the break site. We show that the removal of cross-links drives the exploration of genomic space by the damaged ends, while rates and densities of intact dynamic crosslinking have only a minor role. Local depletion of SMC cross-links proximal to the break site enables the damaged segment to escape the chromosome territory and enhances its ability to explore the genome. Our study reveals a foundational principle by which DSBs can encounter distant regions of sequence homology.

  PublisherDOI

• Centromeres are stress-induced fragile sites

  Current Biology · 2025-02-18 · 4 citations

  articleOpen accessSenior author
  PublisherOA PDFDOI

Recent grants

• Biomechanics of Chromosome Structure and Dynamics In Living Cells

  NSF · $403k · 2005–2009

• MECHANISMS OF MITOTIC SPINDLE ASSEMBLY AND FUNCTION

  NIH · $6.6M · 1978–2020

• Structure and Function of a Eukaryotic Centromere

  NIH · $5.2M · 1983–2022

• NIH Grant K04CA001175

  NIH · $281k · 1992

• NSF-BSF: Defining the relationship between DNA replication kinetics and macromolecular protein assembly at the centromere

  NSF · $900k · 2019–2024

Frequent coauthors

• Elaine Yeh

  71 shared

• Edward D. Salmon

  University of North Carolina at Chapel Hill

  41 shared

• Julian Haase

  40 shared

• Josh Lawrimore

  University of North Carolina at Chapel Hill

  36 shared

• Paul S. Maddox

  University of North Carolina at Chapel Hill

  34 shared

• M. Gregory Forest

  Applied Physical Sciences (United States)

  30 shared

• Andrew D. Stephens

  University of Massachusetts Amherst

  24 shared

• Paula A. Vasquez

  University of South Carolina

  24 shared

Education

• Postdoctoral Fellow, Molecular Biology

  University of California Santa Barbara

  1982

• Ph.D., Biology

  Purdue University

  1980

• B.S., Molecular Biology

  Tulane University

  1975