Cytokinesis is the last step of cell division, when one cell becomes two. Many textbooks describe it as an actomyosin contractile ring that tightens like a belt, but real cells must also remodel their membrane and cortex while the division site shrinks. Our lab views cell cleavage as a 3-D remodeling zone (the furrow plus its surrounding flow field) that must close without getting stuck and jamming. We ask how cells accomplish this by handing off work between RhoA-dependent modules—actomyosin, formin, anillin–septin scaffolds, and later midbody machinery—so that early contraction transitions into a mature midbody ring that supports final separation. We combine quantitative live imaging, controlled perturbations, and modeling to explain why furrows can be slow, pulsed, or asymmetric even when tension is high, and how cells still divide faithfully.

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What is cytokinesis, and why should you care?

 

Every time a cell divides, it must separate its contents and distribute cellular components to two daughters. When cytokinesis fails, cells can become binucleate or genetically unstable—outcomes linked to developmental defects and, in some contexts, cancer and tissue degeneration. Cytokinesis is also a core engine of tissue remodeling: the same principles that let a single cell split help shape embryos, epithelial sheets of cells, and entire organs.

 

 

Our central idea: cleavage is a 3-D remodeling zone, not a 1-D belt

 

Textbooks often describe cytokinesis as a "contractile ring" that tightens like a belt. That’s useful, but incomplete. We study cytokinesis as a 3-D contractility-driven membrane remodeling zone:

 

• a shrinking equatorial membrane–cortex interface where forces act, plus

• a surrounding cortical flow field that moves material into and away from the furrow.

 

In this view, the problem is not simply about “generating force.” It’s about keeping the interface mechanically engaged while it shrinks—in other words, allow closure without getting stuck and jamming.

 

 

Modules and handoffs: how one machine changes gears during division

 

The RhoA GTPase is the universally accepted master regulator of cytokinesis in animal cells. A major view of our lab is that RhoA engages multiple semi-autonomous modules that take turns being most important as the division progresses. Early, the cell must position and engage contractility to build the remodeling zone; later it must stabilize the furrow while allowing it to shrink; and finally it must convert the contractile ring at the center of the remodeling zone into a midbody ring (MR) that supports late events and the eventual physical separation of the daughter cells (called abscission).

 

A simplified “gearbox” view looks like this:

 

1. Engage & load (early furrow): actomyosin and associated regulators establish contractile drive.

2. Stabilize & remodel (mid furrow):  anillo–septin scaffolds organize the membrane-proximal cortex and help manage crowding as the circumference shrinks.

3. Convert to the midbody ring (late): the system transitions from a dynamic contractile structure into a dense, mature MR that can permanently anchor the plasma membrane and coordinate the final separation.

 

We think many classic “stage-specific” phenotypes in cytokinesis make sense as module imbalance: if one module is weakened, others may over-dominate or fail to hand off properly, producing distinctive failure modes (stalling, oscillations, regression, or unstable midbody formation).

 

 

The mechanochemical lens (and the technical term)

 

Mechanically, the furrow is a shrinking interface between cortex and membrane. Molecularly, it’s crowded: many membrane-attached anchors couple force producers and scaffolds to the membrane. The interface is continually being loaded with these anchors by cortical flow from both sides. If anchors cannot be reorganized and cleared as the circumference shrinks, then the interface can “lock up”, even when force is present. In other words, continual loading must be balanced by continual relief, where anchors are cleared from the interface by flowing out. In the lab we use "interface competence" as a technical term for the ability of the shrinking interface to transmit force without locking up, by continuously redistributing these membrane-attached anchors.

 

 

A key pathway we specialize in: the anillo–septin module

 

We have particular expertise in anillin and septins and in how their assemblies shape the cortex and membrane during division. We study how RhoA-dependent "anillo–septin" architectures can act as a membrane-proximal organizing module that helps keep the remodeling zone functional—especially when the system risks becoming stuck and jamming.

 

 

How we do it

 

• Quantitative live imaging to measure organization, turnover, and flows of actomyosin, formins, anillin–septins, and midbody components such as Citron kinase.

• Perturbations to bias specific modules and test predictions (e.g., when force and ingression decouple; when relief/scaffold architectures rescue vs obstruct).

• Constraint-led inference and computational modeling (with collaborators) to build minimal, testable models that predict regime shifts (symmetric vs unilateral/one-sided closure) and the success or failure of the transition to the mature midbody.

 

 

Our goal

 

We aim to extend the actomyosin contractile ring hypothesis to a more realistic 3-D mechanistic, predictive framework: how a cell switches modules and reorganizes its membrane–cortex interface so it can close without jamming, generate asymmetry when needed, and reliably build the midbody ring that completes division.