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"The finding of the double helix thus brought us not only joy but great relief. It was unbelievably interesting and immediately allowed us to make a serious proposal for the mechanism of gene duplication."
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Quick Answer
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Myo19 βintegratesβ with actin by both mechanism (actin-regulated ATPase kinetics) and cellular circuitry (calcium/actin-driven mitochondrial delivery to filopodia tips).
At the molecular level, actin speeds Myo19βs ATPase/Pi-release chemistry and yields a high duty ratio at sufficiently high actin, consistent with ensemble movement rather than single-molecule long processivity.
At the systems level, calcium signaling triggers mitochondrial remodeling and a coordinated handover from a microtubule motor (Kif5B) to actin-driven Myo19, enabling mitochondria to reach filopodia tips during protrusion.
Through recruitment, Myo19 associates with mitochondria via receptors Miro1/2, positioning the actin motor on the organelle so it can couple to actin networks.
Long Answer
How Myo19 interacts with actin & how it integrates in cells
Two levels are required to answer your question without hand-waving:
Molecular coupling (actin β ATPase chemistry)
Actin changes the nucleotide cycle rates (especially Pi release) and increases effective engagement (duty ratio).
EGFβCa2+ remodeling triggers a handover that routes mitochondria into actin-driven filopodia extension where Myo19 is required.
1) Molecular coupling: actin reshapes the Myo19 ATPase cycle
Key actin-dependent rate-limits reported for the human Myo19-3IQ motor domain were: actin-activated Pi release (~172 s^-1) and actin-activated turnover (~3.1 s^-1 head^-1), with modeling that predicts a relatively high duty ratio (~0.8 at high actin).
Engagement/duty ratio
Modeling predicted duty ratio around 0.8 at high actin concentrationsβsupporting βensembleβ behavior as an interpretation rather than strict single-head processivity.
ADP state complexity (uncertainty)
They propose two ADP-bound states contributing to rate-limiting steps; this is model-dependent and inferred rather than directly observed as distinct species.
EGF-induced calcium signaling remodels mitochondria and enables coordinated transport where Kif5B (microtubules) hands off to Myo19 (actin) during filopodia tip extension.
Reported Myo19-mitochondria velocities in body vs filopodia (anterograde/retrograde) support that Myo19 is a functional driver along actin-dependent protrusion geometry.
Critical interpretation / blind spots
These are cell-line and reporter-based observations; motor handover is inferred from perturbations and imaging constraints, and the work acknowledges limitations in generalizing across cell types and in imaging all single-particle behaviors.
Myo19 must be positioned on mitochondria to couple actin-based transport to an organelle cargo. A mechanistic route is provided by Miro1/2: they bind Myo19 and stabilize its mitochondrial association; loss of Miro1/2 (or Myo19) causes mitochondrial mislocalization.
Extra integration note (supportive review): A review summarizes that Miro coordinates mitochondrial movement and that Myo19 can mediate actin-based mitochondrial movement, implying interconnected motor engagement across cytoskeletal systems.
4) A common theme: Myo19 contributes to proper mitochondrial handling during major actomyosin events
During cell division, Myo19 depletion disrupts symmetric mitochondrial partitioning and increases division failure phenotypes, consistent with a role for Myo19 at actomyosin-associated cellular architecture (reported in a HeLa-based functional imaging/RNAi context).
What we know vs what remains uncertain
Known: Actin strongly increases Myo19βs actin-activated Pi release and overall turnover rates, and kinetic modeling supports high duty ratio at high actin.
Known: Calcium signaling in EGF-stimulated cells remodels mitochondria and enables a motor handover resulting in Myo19-dependent actin-driven delivery to filopodia tips.
Known: Miro1/2 bind/stabilize Myo19 on mitochondria, enabling cargo-level integration with cytoskeletal systems.
Uncertain / model-dependent: Proposed ADP-bound state multiplicity in the in vitro kinetic model is inferred and not directly observed as discrete species; extrapolation from motor-domain assays to in vivo ensembles needs validation.
Note: I used only the provided raw research excerpts/data for graphs; any additional mechanistic claims are cited directly to the included sources.
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Hypothesis Graveyard
A βsingle-head, highly processiveβ model for Myo19 is less supported because duty-ratio modeling favors ensemble behavior at high actin rather than long single-molecule run lengths.
A βmicrotubules-onlyβ explanation for filopodia tip mitochondrial delivery is unlikely in the reported EGF system because calcium-dependent handover to Myo19 is central to tip extension/redistribution outcomes.
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