arxiv: 2604.22024 · v1 · submitted 2026-04-23 · ⚛️ physics.bio-ph

Recognition: unknown

Mitochondrial mechanics nucleates axonal jamming and swelling

Ahmed A. Abushawish, Gulcin Pekkurnaz, Padmini Rangamani, Patrick S. Noerr

Pith reviewed 2026-05-08 12:52 UTC · model grok-4.3

classification ⚛️ physics.bio-ph

keywords mitochondrial transportaxonal jammingaxonal swellingfission and fusionagent-based modelmechanical stressorganelle dynamicsneuronal mechanics

0 comments

The pith

Mitochondrial shape and rigidity control whether they jam in axons and cause swelling.

A machine-rendered reading of the paper's core claim, the machinery that carries it, and where it could break.

The paper builds an agent-based model of mitochondria moving inside axons, where collisions arise from motor-driven motion meeting physical crowding. It finds that shape and stiffness decide whether mitochondria pass each other or pile up, and that persistent piles push on the axon wall until it bends outward. Fission makes piles worse by creating many small, clumpy organelles while fusion helps by making longer, stiffer ones that slip through. A sympathetic reader would care because the work ties everyday mitochondrial maintenance directly to the physical integrity of the long cable-like axons that carry signals in the nervous system.

Core claim

Mitochondrial traffic jams emerge from a force balance between active propulsion and steric interactions, and their severity is governed by organelle shape and mechanical properties. Elongated, mechanically rigid mitochondria remain aligned and are transported rapidly, whereas flexible, low-aspect-ratio mitochondria are prone to jamming and accumulation. Incorporating fission and fusion dynamics reveals that fission amplifies transport disruption by generating collision-prone populations, while fusion restores transport by producing anisotropic structures that navigate crowded environments more efficiently. Sustained jamming generates mechanical stress on the axonal membrane, leading to变形和sw

What carries the argument

Agent-based model coupling mitochondrial motility, morphology and lifecycle dynamics to a deformable axonal boundary, through force balance between active propulsion and steric interactions.

If this is right

Elongated rigid mitochondria align and move rapidly through axons without jamming.
Flexible low-aspect-ratio mitochondria jam and accumulate at higher rates.
Increased fission generates more collision-prone mitochondria and worsens jams.
Increased fusion produces elongated shapes that reduce jamming and restore flow.
Persistent jams produce membrane stress that deforms and swells the axon.

Where Pith is reading between the lines

These are editorial extensions of the paper, not claims the author makes directly.

Dysregulated fission-fusion balance could accelerate axonal structural damage in disease through this jamming route.
The model supplies concrete, testable links between organelle population statistics and measurable axon diameter changes.
Similar shape-dependent jamming may occur among other crowded organelles inside narrow cellular processes.

Load-bearing premise

The model assumes that force balance between active propulsion and steric interactions, together with mitochondrial shape and mechanical properties, are the dominant factors governing jamming and axonal deformation.

What would settle it

Live-cell imaging that finds no membrane deformation or swelling at sites of mitochondrial accumulation, regardless of shape or fission-fusion state, would falsify the proposed stress mechanism.

Figures

Figures reproduced from arXiv: 2604.22024 by Ahmed A. Abushawish, Gulcin Pekkurnaz, Padmini Rangamani, Patrick S. Noerr.

**Figure 1.** Figure 1: Motivation and model schematic of mitochondrial transport through neuronal axon. (A) Select examples of axonal swelling from the literature. Axonal membrane in multiple sclerosis (MS) mouse models display various morphologies from uniform cylinders to swellings to rupture. (B) Mitochondrial morphologies corresponding to these axonal states with elongated organelles more present in cylindrical axons and iso… view at source ↗

**Figure 2.** Figure 2: Mitochondria modeled as bidirectionally translated bead-spring chains exhibit jamming in cylindrical axons. (A) Schematic indicating bead spring chain mitochondria undergoing anterograde (green) and retrograde (plum) transport. (B) Simulation snapshots at the time of most severe jamming for low, moderate, and high mitochondrial densities. This time of most severe jamming is different for each mitochondrial… view at source ↗

**Figure 3.** Figure 3: (Caption next page.) 13 view at source ↗

**Figure 3.** Figure 3: Bending stiffness of mitochondria regulates severity of jamming. (A) Schematic demonstrating the order parameters used to analyze characteristic mitochondrial morphologies including the nematic order parameter with respect to the long axis of the channel - Sx and the shape factor - SF. (B) Nematic order as a function of time at the highest density, ϕ = 0.9ϕmax, shows that stiffer filaments experience less… view at source ↗

**Figure 4.** Figure 4: Compact mitochondrial morphologies accentuate jamming severity. (A) Schematic of mitochondrial morphology parameter, Nchain, the number of beads comprising bead spring chain. (B) Minimum nematic order indicates shorter mitochondria become orientationally scrambled. Conversely, longer mitochondria largely retain global orientational order even through jamming. (C) Shape factor at the time of minimum nemat… view at source ↗

**Figure 5.** Figure 5: (Caption next page.) 17 view at source ↗

**Figure 5.** Figure 5: A balance between fission and fusion controls jamming probability. (A) Average chain length indicates high fission rates rapidly give rise to fragmented single bead mitochondria. (B) Nematic order remains close to one for slow fission. Fission gives rise to high variance regimes at sufficient rate constants (kfission > 1 s −1 ), when the population is predominantly Nchain = 1 and Nchain = 2 mitochondria th… view at source ↗

**Figure 6.** Figure 6: Collision induced transport disruption stresses and deforms the axonal membrane. (A) Simulation snapshots of initial anterograde-retrograde collisions (5s - top row), most highly jammed state (10s - middle row), and post collision (15s - bottom row) reveal that intermitochondrial collisions mutually hinder each others motion, thereby nucleating a site of accumulation that grows in time eventually exerting … view at source ↗

read the original abstract

Neuronal function requires precise spatial organization of mitochondria to meet localized energetic demand. However, the physical constraints governing mitochondrial transport in axons remain poorly defined. Bidirectional motor-driven trafficking inherently introduces the potential for collisions, but the implications of these interactions for transport failure and structural damage are not understood. Here, we develop an agent-based model that couples mitochondrial motility, morphology, and lifecycle dynamics to a deformable axonal boundary. We show that mitochondrial traffic jams emerge from a force balance between active propulsion and steric interactions, and that their severity is governed by organelle shape and mechanical properties. Elongated, mechanically rigid mitochondria remain aligned and are transported rapidly, whereas flexible, low-aspect-ratio mitochondria are prone to jamming and accumulation. Incorporating fission and fusion dynamics reveals that fission amplifies transport disruption by generating collision-prone populations, while fusion restores transport by producing anisotropic structures that navigate crowded environments more efficiently. Importantly, we find that sustained jamming generates mechanical stress on the axonal membrane, leading to deformation and swelling. Together, these results establish a physical framework linking mitochondrial dynamics to axonal integrity and provide testable predictions for how dysregulated fission-fusion balance can drive transport failure and structural pathology in neurons.

Editorial analysis

A structured set of objections, weighed in public.

Desk editor's note, referee report, simulated authors' rebuttal, and a circularity audit. Tearing a paper down is the easy half of reading it; the pith above is the substance, this is the friction.

Desk Editor's Note private letter to a colleague

The model links mitochondrial shape and fission-fusion to axonal jamming and swelling through steric forces, but the deformation result depends on the untested claim that other cytoskeletal elements can be ignored.

read the letter

The main point is that this agent-based simulation shows how mitochondrial properties can produce traffic jams that then push on and deform the axonal membrane. Rigid, elongated mitochondria move through better while flexible or round ones jam more easily, and fission makes the jams worse while fusion helps clear them. The swelling comes from sustained steric pressure once the jam builds up. That chain is the central new claim.

Referee Report

1 major / 1 minor

Summary. The paper introduces an agent-based model that couples mitochondrial motility, morphology, and fission-fusion dynamics to a deformable axonal boundary. It claims that mitochondrial jamming emerges from the force balance between active motor-driven propulsion and steric interactions, modulated by organelle shape and mechanical properties. Elongated, rigid mitochondria are transported efficiently, while flexible, low-aspect-ratio ones are prone to jamming. Fission increases disruption, fusion restores transport, and sustained jamming produces mechanical stress leading to axonal swelling and deformation.

Significance. If the model's assumptions hold, this establishes a physical link between mitochondrial dynamics and axonal pathology, with implications for understanding neurodegenerative conditions involving transport defects. The model generates specific, testable predictions regarding the effects of fission-fusion imbalance. Strengths include the integration of morphology, mechanics, and boundary deformation in a single framework. However, the results are simulation-based and would benefit from direct experimental validation to confirm the dominance of the modeled interactions.

major comments (1)

[Model description and results on membrane deformation] Model description and results on membrane deformation: The claim that sustained jamming generates mechanical stress on the axonal membrane, leading to deformation and swelling, depends on the untested assumption that steric and mitochondrial forces dominate over other cytoskeletal elements such as microtubules, actin cortex, and neurofilaments. No quantitative bounds, sensitivity analysis, or comparison showing that inclusion of these elements would not alter the deformation threshold are provided. This assumption is load-bearing for the headline result.

minor comments (1)

[Abstract] The abstract mentions 'testable predictions' but does not explicitly state them; including one or two key predictions would improve clarity for readers.

Simulated Author's Rebuttal

1 responses · 0 unresolved

We thank the referee for their constructive review and for acknowledging the potential significance of our agent-based model in connecting mitochondrial dynamics to axonal pathology. We address the single major comment below and will revise the manuscript accordingly to strengthen the presentation of our assumptions and results.

read point-by-point responses

Referee: The claim that sustained jamming generates mechanical stress on the axonal membrane, leading to deformation and swelling, depends on the untested assumption that steric and mitochondrial forces dominate over other cytoskeletal elements such as microtubules, actin cortex, and neurofilaments. No quantitative bounds, sensitivity analysis, or comparison showing that inclusion of these elements would not alter the deformation threshold are provided. This assumption is load-bearing for the headline result.

Authors: We appreciate the referee identifying this foundational assumption in our model of axonal deformation. The framework is constructed to isolate the mechanical consequences of mitochondrial jamming and steric interactions with a deformable boundary, without explicit representation of microtubules, actin cortex, or neurofilaments. We agree that these cytoskeletal elements contribute to axonal mechanics in vivo and could modulate deformation thresholds. Incorporating them fully would require a substantially more complex multi-component biomechanical model beyond the current scope. In the revised manuscript we will add an explicit limitations subsection that states the assumption clearly, supplies order-of-magnitude estimates comparing typical mitochondrial propulsion forces to reported cytoskeletal stiffnesses, and includes new sensitivity simulations in which boundary stiffness is varied over a physiologically plausible range. These additions will provide quantitative bounds on the deformation threshold and clarify the conditions under which mitochondrial forces remain dominant. revision: yes

Circularity Check

0 steps flagged

Model simulation produces emergent jamming and swelling from explicit force-balance rules

full rationale

The paper constructs an agent-based model with explicit rules for mitochondrial motility, morphology, fission/fusion, and force balance between active propulsion and steric interactions acting on a deformable axonal boundary. Reported outcomes (jamming severity governed by shape/mechanics, sustained jamming producing membrane stress and swelling) are simulation results under those rules rather than quantities fitted to or defined by the target phenomenon. No self-definitional equations, fitted-input predictions, or load-bearing self-citations that reduce the central claim to its own inputs appear in the abstract or model description. The derivation is therefore self-contained as a forward simulation.

Axiom & Free-Parameter Ledger

1 free parameters · 1 axioms · 0 invented entities

The model rests on standard biophysical assumptions about motor-driven transport and steric interactions, with parameters for mitochondrial shape, rigidity, and boundary deformability introduced for this study; full details unavailable from abstract.

free parameters (1)

mitochondrial aspect ratio and rigidity parameters
Shape and mechanical properties are central to the jamming outcome but specific values and fitting procedure not provided in abstract.

axioms (1)

domain assumption Force balance between active propulsion and steric interactions governs mitochondrial movement and jamming.
Directly invoked to explain emergence of traffic jams from motility and interactions.

pith-pipeline@v0.9.0 · 5516 in / 1376 out tokens · 62995 ms · 2026-05-08T12:52:15.706352+00:00 · methodology

discussion (0)

Reference graph

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