GO:0060002 plus-end directed microfilament motor activity: Mechanism, Genes and Research Methods
Research-grade guide for scientists and biopharma professionals
Key Takeaways
• GO:0060002 describes ATP-hydrolysis-driven motor activity that moves cargo along actin microfilaments toward the plus (barbed) end.
• Myosin superfamily motors, especially myosin VI mutants engineered to move toward the plus end, are experimental tools for dissecting directionality.
• Plus-end-directed actin motors cooperate with microtubule motors during organelle transport in pigment cells.
• Myosin IIIa transports espin 1 to stereocilia plus ends to boost actin elongation in inner ear hair cells.
• Bidirectional movement of cytoplasmic dynein-associated structures shows that actin and microtubule motors are coordinated in vivo.
• Cortical capture of astral microtubules by Bud6p illustrates plus-end-directed motor-like priming of spindle polarity in yeast.
Description
Plus-end directed microfilament motor activity (GO:0060002) is a molecular function in which a motor protein converts ATP hydrolysis into directed movement along an actin filament toward its plus, or barbed, end. This activity is essential for processes that require precise delivery of cargo to actin-rich structures, such as filopodia, stereocilia, and endosome clusters. Unlike minus-end-directed myosins, plus-end-directed motors move cargo toward the fast-growing end of actin filaments, a directionality that is critical for assembly and signaling at the cell periphery. Researchers study this activity to understand how cells organize actin-based transport, how motor directionality is determined, and how defects contribute to disease. The function is experimentally tractable because mutant myosins can be engineered to reverse direction, providing direct tests of plus-end-directed motility in living cells. In addition, plus-end-directed actin motors cooperate with microtubule motors during organelle transport, revealing integrated transport networks. This article synthesizes authoritative GO annotations and verified PubMed literature to explain the mechanism, genes, disease links, and research methods for GO:0060002.
plus-end directed microfilament motor activity At A Glance
| GO ID | GO:0060002 |
|---|---|
| GO term | plus-end directed microfilament motor activity |
| Ontology | molecular_function |
| Synonym | barbed-end directed actin-filament motor activity; plus-end directed actin filament motor activity; plus-end directed actin-filament motor activity |
| Major function | ATP-hydrolysis-driven movement of cargo along actin filaments toward the plus (barbed) end |
| Directionality | Toward the plus end, the end that preferentially adds actin monomers |
| Energy source | ATP hydrolysis |
| Example motor | Mutant plus-end-directed myosin VI |
| Related process | Filopodia formation, endosome clustering, stereocilia elongation |
What Is GO:0060002?
GO:0060002 is defined as a motor activity that generates movement along a microfilament toward the plus end, driven by ATP hydrolysis. The plus end of an actin filament is the end that preferentially adds actin monomers, also called the barbed end. This term captures the directionality and energy-coupling of the motor, not the identity of the motor protein itself.
Why Is plus-end directed microfilament motor activity Important in Cell Biology?
Plus-end directed microfilament motor activity is important because it governs how cells deliver materials to the growing, plus ends of actin filaments, which are concentrated at the leading edge, filopodia tips, and stereocilia tips. This activity supports actin assembly, sensory hair cell function, and organelle positioning, and it must be coordinated with microtubule-based transport. Defects in plus-end-directed actin motors or their cargo adaptors can disrupt these processes and contribute to disease, making GO:0060002 a key functional node for cell biology and translational research.
• Drives cargo delivery to actin plus ends during filopodia formation and endosome clustering.
• Supports stereocilia elongation by transporting espin 1 to actin filament plus ends in hair cells.
• Cooperates with microtubule motors during organelle transport in melanophores.
• Contributes to bidirectional movement of cytoplasmic dynein-associated structures in vivo.
• Helps prime spindle polarity through cortical capture of astral microtubules in yeast.
• Provides a mechanistic handle for engineering motor directionality in living cells.
• Links actin cytoskeleton dynamics to sensory and transport functions.
• Offers targets for studying cytoskeletal transport defects in disease models.
Molecular Mechanism of plus-end directed microfilament motor activity
ATP hydrolysis and force generation
In simple terms: The motor burns ATP to move along actin in one direction.
Plus-end directed microfilament motor activity is powered by ATP hydrolysis, which drives conformational changes that produce movement along the actin filament toward the plus end. This coupling of chemical energy to mechanical work is the defining feature of the GO:0060002 molecular function.
Directionality toward the barbed end
In simple terms: The motor walks toward the fast-growing end of the actin filament.
The plus end of an actin filament is the barbed end that preferentially adds actin monomers, and plus-end-directed motors move cargo toward this end. Mutant plus-end-directed myosin VI demonstrates that directionality can be reversed by altering the motor domain, providing direct evidence for plus-end-directed motility in cells.
Cargo transport to actin-rich structures
In simple terms: The motor carries cargo to places where actin is growing.
Plus-end-directed myosin VI mutants induce filopodia formation and endosome clustering, showing that this activity delivers cargo to actin-rich peripheral structures. Myosin IIIa similarly transports espin 1 to the plus ends of actin filaments to boost stereocilia elongation.
Coordination with microtubule motors
In simple terms: Actin motors work together with microtubule motors to move organelles.
Myosin cooperates with microtubule motors during organelle transport in melanophores, indicating that plus-end-directed actin motor activity is integrated with microtubule-based transport. Cytoplasmic dynein-associated structures move bidirectionally in vivo, further supporting coordinated motor activity.
Cortical capture and polarity priming
In simple terms: Motor-like capture at the cortex helps set up cell polarity.
In S. cerevisiae, cortical Bud6p primes spindle polarity by capturing astral microtubules, a process that involves plus-end-directed motor-like activity at the cortex. This illustrates how plus-end-directed microfilament motor activity contributes to spatial organization beyond simple cargo transport.
Key Genes Involved in GO:0060002 plus-end directed microfilament motor activity
The following genes and proteins are experimentally linked to plus-end directed microfilament motor activity or its coordination with other motors.
| Gene | Major Role | Research Relevance |
|---|---|---|
| MYO6 | Myosin VI motor; mutant plus-end-directed form induces filopodia and endosome clustering | Directionality engineering and cargo transport studies |
| MYO3A | Myosin IIIa transports espin 1 to actin plus ends in stereocilia | Hearing and stereocilia elongation research |
| ESPN | Espin 1 cargo delivered to plus ends by myosin IIIa | Actin bundling and stereocilia maintenance |
| DYNC1H1 | Cytoplasmic dynein heavy chain; associated structures move bidirectionally | Coordination of actin and microtubule transport |
| BUD6 | Cortical protein priming spindle polarity via astral microtubule capture | Yeast polarity and spindle positioning |
| ACTB | Actin filament subunit; track for plus-end-directed motors | Cytoskeleton dynamics and motor assays |
| ACTG1 | Actin filament subunit in motile and sensory cells | Stereocilia and cytoskeletal transport |
| MYO7A | Myosin superfamily member in actin-based transport | Sensory cell actin motor research |
| MYO5A | Myosin V family motor in actin-based cargo transport | Organelle transport coordination |
| MYO10 | Myosin X in filopodia formation | Filopodia and plus-end actin dynamics |
| RAB5 | Endosomal marker in endosome clustering assays | Endosome transport and clustering |
| RAB7 | Late endosomal marker in motor transport studies | Endosome positioning |
| CDC42 | Regulator of actin assembly and filopodia | Filopodia formation signaling |
| ARP2/3 | Actin nucleation complex in plus-end actin assembly | Actin network assembly |
| PROFILIN | Actin monomer binding protein in filament elongation | Actin plus-end growth assays |
| COFILIN | Actin severing and turnover factor | Actin dynamics regulation |
| TWF1 | Actin depolymerizing factor in cytoskeletal turnover | Actin filament remodeling |
| WASF1 | WASP family actin nucleation regulator | Filopodia and actin assembly |
How Is plus-end directed microfilament motor activity Regulated?
Plus-end directed microfilament motor activity is regulated by motor domain structure, cargo adaptors, and coordination with microtubule motors. Mutations in the myosin VI motor domain can reverse directionality, showing that intrinsic motor sequence controls plus-end versus minus-end movement. Cargo binding and cellular context, such as endosome clustering and filopodia formation, further modulate where and when this activity occurs. In stereocilia, myosin IIIa-dependent delivery of espin 1 to plus ends is regulated to match actin elongation needs. Coordination with microtubule motors in melanophores indicates that plus-end-directed actin motor activity is tuned within a broader transport network.
plus-end directed microfilament motor activity and Human Disease
| Gene | Disease / Biology | Potential Experimental Model |
|---|---|---|
| MYO3A | Hearing loss and stereocilia elongation defects | Knockout or point-mutation in hair cell models |
| MYO6 | Cytoskeletal transport and endosome clustering defects | Plus-end-directed mutant knock-in in cultured cells |
| ESPN | Actin bundling defects in sensory cells | Tagged knock-in to track plus-end delivery |
| DYNC1H1 | Bidirectional organelle transport defects | Knockout or overexpression in pigment cells |
| BUD6 | Spindle polarity defects | Yeast knockout and live imaging |
Hearing loss and stereocilia defects
Myosin IIIa boosts stereocilia elongation by transporting espin 1 to the plus ends of actin filaments, and disruption of this plus-end-directed delivery can impair hair cell actin structures relevant to hearing.
Cytoskeletal transport disorders
Plus-end-directed myosin VI mutants alter filopodia formation and endosome clustering, linking this motor activity to cytoskeletal organization defects. Coordination with microtubule motors during organelle transport further suggests that imbalance in plus-end-directed actin motility can perturb intracellular trafficking.
Cell polarity and division defects
Cortical Bud6p primes spindle polarity by capturing astral microtubules in S. cerevisiae, a process involving plus-end-directed motor-like activity that, when disrupted, affects spindle positioning. This provides a model for understanding polarity defects in higher cells.
From plus-end directed microfilament motor activity-Related Genes to Experimental Models
| Research Question | Suitable Model |
|---|---|
| Does a candidate motor move toward the actin plus end? | Point-mutation of motor domain with live imaging |
| What cargo is delivered to plus ends? | Tagged knock-in of cargo and motor |
| Is the motor required for filopodia formation? | Knockout or knockdown in cultured cells |
| How does plus-end motor activity coordinate with microtubules? | Overexpression and dual-color imaging |
| Does the motor regulate spindle polarity? | Yeast knockout and cortical capture assays |
| Can directionality be reversed? | Engineered plus-end-directed mutant knock-in |
How to Study the plus-end directed microfilament motor activity Process
| Method | What It Measures | Typical Application |
|---|---|---|
| Live-cell fluorescence imaging | Direction and speed of motor movement | Plus-end-directed motility assays |
| Endosome clustering assay | Cargo aggregation at plus ends | Mutant myosin VI function |
| Filopodia formation assay | Actin-based protrusion induction | Plus-end-directed motor activity |
| Stereocilia elongation measurement | Actin plus-end delivery and growth | Myosin IIIa and espin 1 studies |
| Organelle transport tracking | Coordination with microtubule motors | Melanophore transport assays |
| Bidirectional movement analysis | Dynein-associated structure dynamics | In vivo transport studies |
| Spindle polarity imaging | Astral microtubule capture | Yeast polarity assays |
| Co-localization microscopy | Motor-cargo association | Cargo identification |
Live-cell imaging of motor directionality
Live-cell imaging of fluorescently tagged motors and cargo allows direct observation of plus-end-directed movement along actin filaments. Mutant plus-end-directed myosin VI provides a positive control for directionality assays.
Cargo tracking and endosome clustering assays
Endosome clustering and filopodia formation can be quantified to measure plus-end-directed motor activity in cells expressing mutant motors. Co-localization with endosomal markers such as RAB5 and RAB7 helps define cargo identity.
Stereocilia elongation and actin plus-end delivery
Myosin IIIa-dependent transport of espin 1 to actin plus ends can be studied in hair cell models to link plus-end-directed activity to stereocilia elongation.
Coordination with microtubule transport
Melanophore organelle transport assays reveal cooperation between myosin and microtubule motors, and bidirectional movement of dynein-associated structures can be tracked in vivo.
How CRISPR Can Be Used to Study GO:0060002 plus-end directed microfilament motor activity
Knockout
CRISPR knockout of MYO3A or MYO6 can test whether plus-end-directed microfilament motor activity is required for stereocilia elongation or endosome clustering. Loss-of-function models help define the contribution of each motor to actin plus-end transport.
Point Mutation
Point mutations in the motor domain can reverse or abolish directionality, as shown for plus-end-directed myosin VI mutants. CRISPR point-mutation models allow precise testing of residues that control plus-end versus minus-end movement.
Knock-in
Tagged knock-in of motors and cargo such as espin 1 enables real-time tracking of plus-end-directed delivery in native cells. Knock-in of mutant motors can also recreate disease-relevant directionality changes.
Overexpression
Overexpression of plus-end-directed motors or their cargo adaptors can amplify actin-based transport and reveal dominant effects on filopodia and organelle positioning. Overexpression models are useful for testing coordination with microtubule motors.
How EDITGENE Supports plus-end directed microfilament motor activity Research
Researchers studying plus-end directed microfilament motor activity-related genes often need to determine whether a candidate gene is causally involved in actin-based transport, directionality, or cargo delivery. EDITGENE provides CRISPR-based cell models and screening services to test these hypotheses with publication-ready rigor.
Contact EDITGENE today to design your custom CRISPR model for plus-end directed microfilament motor activity research.
Frequently Asked Questions About plus-end directed microfilament motor activity
What is plus-end directed microfilament motor activity?
It is an ATP-hydrolysis-driven motor activity that moves cargo along actin filaments toward the plus (barbed) end, defined as GO:0060002.
What genes are involved in plus-end directed microfilament motor activity?
Genes include MYO6, MYO3A, ESPN, DYNC1H1, and BUD6, among others linked to actin-based transport.
Which motor protein moves toward the plus end of actin filaments?
Mutant plus-end-directed myosin VI is a well-characterized example that moves toward the plus end and induces filopodia and endosome clustering.
How is plus-end directed microfilament motor activity powered?
It is powered by ATP hydrolysis, which drives conformational changes that produce movement along the actin filament.
What is the difference between plus-end and minus-end directed actin motors?
Plus-end-directed motors move toward the barbed end that preferentially adds actin monomers, whereas minus-end-directed motors move toward the opposite end.
What diseases are linked to plus-end directed microfilament motor activity?
Disruption of myosin IIIa-dependent espin 1 delivery to stereocilia plus ends is linked to hearing-related actin defects, and altered myosin VI activity affects cytoskeletal transport.
How do researchers study plus-end directed microfilament motor activity?
They use live-cell imaging, endosome clustering assays, filopodia formation assays, and stereocilia elongation measurements.
Does plus-end directed microfilament motor activity cooperate with microtubule motors?
Yes, myosin cooperates with microtubule motors during organelle transport in melanophores, and dynein-associated structures move bidirectionally in vivo.
What is the GO ID for plus-end directed microfilament motor activity?
The GO ID is GO:0060002.
Can CRISPR be used to study plus-end directed microfilament motor activity?
Yes, CRISPR knockout, point mutation, knock-in, and overexpression models can test motor directionality and cargo delivery.
Conclusion
Plus-end directed microfilament motor activity (GO:0060002) is a defined molecular function that couples ATP hydrolysis to movement along actin filaments toward the barbed end. It underlies filopodia formation, endosome clustering, stereocilia elongation, and coordinated organelle transport with microtubule motors. Studying this activity with CRISPR-based models and imaging assays provides mechanistic insight into cytoskeletal transport and related disease processes.
References
- 1. Masters TA et al.. 2017. Filopodia formation and endosome clustering induced by mutant plus-end-directed myosin VI.. Proc Natl Acad Sci U S A 114(7):1595-1600 PMID: 28143933
- 2. Ma S et al.. 2002. Cytoplasmic dynein-associated structures move bidirectionally in vivo.. J Cell Sci 115(Pt 7):1453-60 PMID: 11896193
- 3. Ten Hoopen R et al.. 2012. Mechanism for astral microtubule capture by cortical Bud6p priming spindle polarity in S. cerevisiae.. Curr Biol 22(12):1075-83 PMID: 22608510
- 4. Rogers SL et al.. 1998. Myosin cooperates with microtubule motors during organelle transport in melanophores.. Curr Biol 8(3):161-4 PMID: 9443916
- 5. Salles FT et al.. 2009. Myosin IIIa boosts elongation of stereocilia by transporting espin 1 to the plus ends of actin filaments.. Nat Cell Biol 11(4):443-50 PMID: 19287378
