LEKR1

Model summary

A soluble human adaptor that organizes mitotic machinery by using a single LEKR1-family scaffold to bind and stabilize spindle-associated assemblies. It operates primarily through multivalent protein interactions to promote central spindle formation and maturation, thereby ensuring accurate spindle assembly and successful cytokinesis. The protein cycles between the cytosol and nucleoplasm and accumulates at centrosomes during mitosis, coordinating spatial assembly pathways that couple microtubule architecture to cell division.

Predicted Gene Ontology terms

1. 01

   I begin with the InterPro architecture: IPR038799 (Protein LEKR1 family) spans residues 1–127 and covers the entire polypeptide, indicating a single-domain, non-enzymatic scaffold/adaptor typical of the LEKR1 family.

   Full-length coverage by a family signature and the absence of catalytic or transmembrane domains argue that this protein functions through selective macromolecular interactions rather than enzymatic chemistry. Such single-domain adaptors commonly mediate assembly and spatial control of cytoskeletal and cell-cycle machineries by binding partners; this architecture therefore causes a primary molecular function of protein binding (GO:0005515).

2. 02

   From this binding-centric core, I infer its role in mitosis.

   The LEKR1-family scaffold is suited to organize and stabilize complexes that build and remodel the spindle and its central spindle. This directly supports participation in mitotic spindle midzone assembly (GO:0051256), where midzone crosslinkers and motors are nucleated and stabilized. By promoting midzone maturation, the adaptor indirectly drives mitotic cytokinesis (GO:0000281), because a properly assembled central spindle is the prerequisite for furrow ingression and abscission. Its contribution to assembling and maintaining a robust bipolar apparatus also underpins mitotic spindle assembly (GO:0090307). Together, these processes describe a coherent pathway: scaffolded midzone assembly leads to central spindle formation, which in turn enables cytokinesis.

3. 03

   Cellular localization follows from this mitotic itinerary.

   A soluble adaptor without transmembrane features resides in the cytosol (GO:0005829), where spindle components are synthesized and pre-assemble. During interphase and early mitosis, such scaffolds often shuttle through the nucleoplasm (GO:0005654), consistent with soluble, cell-cycle-regulated nuclear-cytoplasmic exchange. As cells enter mitosis, the adaptor concentrates at the centrosome (GO:0005813), a logical waypoint for spindle pole organization and midzone specification. This spatial progression—cytosol and nucleoplasm to centrosomes—matches the observed dynamics of spindle assembly and midzone formation.

4. 04

   Mechanistically, I hypothesize that the LEKR1-family domain forms a compact interaction hub that recruits and stabilizes central spindle modules.

   By binding midzone organizers and motors, it likely enhances the fidelity of spindle midzone assembly and ensures timely cytokinesis. In this model, the adaptor transiently associates with centralspindlin and associated Rho pathway regulators to coordinate microtubule bundling and contractile ring coupling. Likely partners include centralspindlin components and midzone crosslinkers; these assemblies explain how a single-domain binding scaffold can causally drive spindle midzone assembly, mitotic spindle assembly, and ultimately cytokinesis.