A surreal illustration of a Kinesin-13 protein at work, dismantling a microtubule within a cell.

Unlocking the Secrets of Kinesin-13: How These Tiny Motors Shape Our Cells

Jordan Keane in Science & Nature September 2025 • 4 min read.

"Dive into the world of Kinesin-13 proteins, the microscopic demolition crew responsible for dismantling microtubules and orchestrating essential cellular processes."

Imagine a bustling city where roads are constantly being built and torn down to manage traffic flow. Inside our cells, a similar process occurs with microtubules, the structural highways that support cell shape, movement, and division. Orchestrating this dynamic construction and demolition are Kinesin-13 proteins, a specialized family of molecular motors with a knack for dismantling microtubules.

These tiny biological machines are part of the larger kinesin superfamily, all powered by ATP, the cell's energy currency. But unlike other kinesins that transport cargo along microtubules, Kinesin-13s are microtubule depolymerases, meaning they break down these structures. This unique ability allows them to regulate a variety of essential cellular functions.

From ensuring accurate chromosome segregation during cell division to maintaining the delicate architecture of neurons and supporting the function of cilia, Kinesin-13s play crucial roles. Understanding their structure and function is vital for unraveling the complexities of cell biology and developing new therapeutic strategies.

Kinesin-13s: The Specialist Microtubule Depolymerisers

A surreal illustration of a Kinesin-13 protein at work, dismantling a microtubule within a cell.

Kinesin-13s are unique in their ability to destabilize microtubules, structures crucial for cell division and intracellular transport. Unlike most kinesins, which move along microtubules, Kinesin-13s diffuse along them, breaking them down from both ends. This depolymerisation activity is essential for various cellular processes.

There are four main Kinesin-13 family members in mammals: KIF2A, KIF2B, KIF2C (also known as MCAK), and KIF24. Although they share a conserved motor domain, their N- and C-terminal regions differ, giving them specific functions and targeting abilities. This divergence allows each member to contribute uniquely to cellular dynamics.

KIF2A: Plays a critical role in neuronal development by regulating axonal pruning, ensuring proper nerve cell structure.
KIF2B: Involved in correcting microtubule-kinetochore attachments, although its exact role is still debated.
KIF2C (MCAK): A highly studied member, essential for chromosome segregation and kinetochore-microtubule attachments.
KIF24: Regulates the length of cilia, which are essential for cell signaling and movement.

The most extensively researched Kinesin-13 is MCAK/KIF2C. First identified at the inner centromeres of chromosomes, MCAK contributes to the correct formation of kinetochore-microtubule attachments, which are essential for accurate chromosome segregation during cell division. Its activity at centromeres is regulated by Aurora B kinase, ensuring proper timing and coordination during mitosis.

Unanswered Questions and Future Directions

While significant progress has been made in understanding Kinesin-13s, several questions remain. What specific molecular characteristics give the Kinesin-13 family its specialized depolymerizing activity? How do these kinesins distinguish between microtubule ends and the microtubule lattice? Why do Kinesin-13s function as dimers in cells, even though monomeric constructs can depolymerize microtubules in vitro? Answering these questions will not only deepen our understanding of cell biology but also pave the way for new therapeutic interventions targeting diseases involving microtubule dysfunction.

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Everything You Need To Know

What is the primary function of Kinesin-13 proteins?

Kinesin-13 proteins are primarily responsible for dismantling microtubules, which are essential for various cellular processes. They are microtubule depolymerases, meaning they break down microtubules, unlike other kinesins that transport cargo along them. This depolymerization activity is crucial for regulating cell division, neuronal development, and other essential cellular functions.

How do Kinesin-13s differ from other members of the kinesin superfamily?

Unlike most kinesins, which move along microtubules, Kinesin-13s diffuse along microtubules and break them down from both ends. This unique ability to depolymerize microtubules distinguishes them from other kinesins. Kinesin-13s are powered by ATP, like all members of the kinesin superfamily, but their specific role in dismantling microtubules makes them specialized molecular motors with a key role in cellular dynamics.

What are the main roles of the different Kinesin-13 family members?

There are four main Kinesin-13 family members in mammals: KIF2A, KIF2B, KIF2C (MCAK), and KIF24. KIF2A is involved in neuronal development and axonal pruning. KIF2B plays a role in correcting microtubule-kinetochore attachments. KIF2C (MCAK) is essential for chromosome segregation. KIF24 regulates the length of cilia, which are critical for cell signaling and movement. Each member's unique structure and function allows them to contribute to cellular dynamics in specific ways.

Why is understanding Kinesin-13s important for medicine?

Understanding Kinesin-13s is vital for advancing medicine because they are involved in several critical cellular processes. They play roles in cell division, neuronal development, and the function of cilia. Because of their role, dysfunctions in Kinesin-13s can lead to various diseases. Research into these proteins may lead to the development of new therapeutic strategies and interventions targeting diseases associated with microtubule dysfunction, such as cancer and neurological disorders.

What are some of the unanswered questions about Kinesin-13s and what are the implications of these questions?

Several questions about Kinesin-13s remain unanswered. Scientists are working to understand the molecular characteristics that give the Kinesin-13 family their depolymerizing activity, how they distinguish between microtubule ends and the microtubule lattice, and why they function as dimers in cells. Answering these questions would deepen the understanding of cell biology and potentially uncover novel therapeutic interventions. For example, understanding the specific mechanisms involved in microtubule depolymerization could provide targets for drugs that interfere with cell division in cancer cells, or that promote neuron health in neurodegenerative conditions.