CLASP-dependent microtubule stabilization generates microtubule-based protrusive forces during Drosophila epithelial morphogenesis.

Tissue morphogenesis requires tight coordination between biochemical signaling and mechanical forces that sculpt cells and tissues. While actomyosin networks are well-established force generators, microtubule-based mechanics have recently emerged as crucial contributors to tissue remodeling. Yet, how dynamic microtubules, whose plus ends undergo compression-induced catastrophes that limit their load-bearing capacity, generate forces in vivo remains unclear. Here, we identify Orbit, the Drosophila cytoplasmic linker-associated protein (CLASP) homolog, as a key factor that stabilizes non-centrosomal microtubule plus ends in vivo, enabling them to sustain mechanical loads. In the pupal wing epithelium, these Orbit-stabilized, planar-polarized microtubules are consistent with a role in counteracting actomyosin contractility and promoting tissue elongation. Loss of Orbit increases catastrophe frequency and disrupts epithelial elongation, whereas Orbit overexpression enhances microtubule rescues by suppressing catastrophes, thereby promoting cell anisotropy and tissue extension. Moreover, Orbit-mediated stabilization is sufficient to induce microtubule-dependent, filopodia-like protrusions independent of actin. Together, these findings establish CLASP-dependent microtubule stabilization as a key mechanism linking polymerization dynamics to epithelial morphogenesis.