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Nonmuscle myosin 2 filaments are processive in cells

  • Eric A. Vitriol(corresponding author)
    ,
  • Melissa A. Quintanilla
    ,
  • Joseph J. Tidei
    ,
  • Lee D. Troughton
    ,
  • Abigail Cody
    ,
  • Bruno A. Cisterna
*Corresponding author for this work
Scholary Output:
Contribution to journal
Article
Peer-review

Open access

Abstract

Directed transport of cellular components is often dependent on the processive movements of cytoskeletal motors. Myosin 2 motors predominantly engage actin filaments of opposing orientation to drive contractile events and are therefore not traditionally viewed as processive. However, recent in vitro experiments with purified nonmuscle myosin 2 (NM2) demonstrated myosin 2 filaments could move processively. Here, we establish processivity as a cellular property of NM2. Processive runs in central nervous system-derived CAD cells are most apparent on bundled actin in protrusions that terminate at the leading edge. We find that processive velocities in vivo are consistent with in vitro measurements. NM2 makes these processive runs in its filamentous form against lamellipodia retrograde flow, though anterograde movement can still occur in the absence of actin dynamics. Comparing the processivity of NM2 isoforms, we find that NM2A moves slightly faster than NM2B. Finally, we demonstrate that this is not a cell-specific property, as we observe processive-like movements of NM2 in the lamella and subnuclear stress fibers of fibroblasts. Collectively, these observations further broaden NM2 functionality and the biological processes in which the already ubiquitous motor can contribute.

Publication Information

Output type

Scholary Output:
Contribution to journal
Article
Peer-review

Original language

English (US)

Pages from-to (Number of pages)

Pages 3678-3689 (12 pages)

Journal (Volume, Issue Number)

Biophysical Journal (Volume 122, Issue 18)

Publication milestones

  • Accepted/In press - 2023
  • Published - 09/19/2023

Publication status

Published - 09/19/2023

ISSN

0006-3495

Publication IDs

  • Scopus: 85163311468
  • PubMed: 37218133

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Funding Details

This work is dedicated to the memory of Dr. Ken Jacobson. Research reported in this publication was supported by the Maximizing Investigators’ Research Award (MIRA) (R35) from the National Institute of General Medical Sciences (NIGMS) of the National Institutes of Health (NIH) under grant number R35GM137959 to E.A.V. and R35GM138183 to J.R.B. and Graduate Research Fellowship (GRFP) from the National Science Foundation (NSF) under grant number DGE-1842190 to M.A.Q. P.W.O. is supported in part by a National Science Foundation CAREER Award #2000554 and National Institutes of Health (NIH) National Institute of Allergy and Infectious Disease (NIAID) (Award # P01-AI02851). The authors declare no competing interests. This work is dedicated to the memory of Dr. Ken Jacobson. Research reported in this publication was supported by the Maximizing Investigators’ Research Award (MIRA) (R35) from the National Institute of General Medical Sciences (NIGMS) of the National Institutes of Health (NIH) under grant number R35GM137959 to E.A.V. and R35GM138183 to J.R.B., and Graduate Research Fellowship (GRFP) from the National Science Foundation (NSF) under grant number DGE-1842190 to M.A.Q. P.W.O. is supported in part by a National Science Foundation CAREER Award # 2000554 and National Institutes of Health (NIH) National Institute of Allergy and Infectious Disease (NIAID) (Award # P01-AI02851 ).
FundersFunding numbers
NIGMS
-
NIAID
P01-AI02851
NSF
DGE-1842190, 2000554
NIH
R35GM137959, R35GM138183