bioRxiv Science⌕ Search

bioRxiv · 10.64898/2026.10.31.763351

A developmentally scheduled inhibitory polarity circuit centers the stomatal pore

Abstract

Symmetry in living systems often arises from coordinated asymmetries at smaller scales. The guard cells of stomata--bilaterally symmetric epidermal valves that mediate plant-atmosphere gas exchange--show coordinated asymmetries in pore placement and wall modification. Stomatal form and function are deeply conserved, yet molecular mechanisms defining coordinated cellular asymmetry are unknown. Here we show that pore position arises from a combination of pole avoidance and gradient centering in the membranes and wall dividing sister guard cells. Boundaries are established by spatiotemporal restriction of the receptor-like kinase MUSTACHES (MUS), which directs the disordered polarity protein OCTOPUS-LIKE2 (OPL2) to pore-forming regions. OPL2 peaks correspond to a focus of microtubules, and, from this position, the pore emerges. Experimental rewiring of the MUS-OPL2 polarity module profoundly impacts stomatal morphogenesis, eliminating, shifting, or even redirecting the pore to the opposite wall. These findings reveal a stomata-specific integration and elaboration of core polarity and centering programs, and challenge previous models of stomatal morphogenesis.

Explore related subjects

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

Lebecq, A., Wallner, E.-S., Bergmann, D. C.. 2026-11-02. A developmentally scheduled inhibitory polarity circuit centers the stomatal pore. https://doi.org/10.64898/2026.10.31.763351

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related preprints

PPI-Rescue: restoration of eye development via functional reconstitution of a transcription complex.

The activity of transcription factors (TFs) can be modulated through protein-protein interactions (PPIs) with cofactors which can serve to enhance, repress or alter the specificity of TF function. Current genetic and molecular approaches such as knockout and overexpression studies are likely to affect all possible activities of a TF, presenting a dilemma when attempting to parse out how TFs function within a cell. Hence, there is a need to devise a technique that will allow for mechanistic insight to be gained into the function(s) of discrete transcription complexes. Herein we report ''PPI-Rescue'', an approach that leverages bespoke mutations in TFs and the selective reconstitution of specific complexes to study the molecular properties and biological functions of discrete transcription complexes in vitro and in vivo. We demonstrate PPI-Rescue using the conserved Drosophila transcription factor Sine oculis (So) and cofactor Eyes Absent (Eya). To validate this approach, we engineered a missense mutation, So{Delta}Eya (C110S), that selectively abrogates PPI-Eya to show that PPI-Eya is necessary for the transcriptional activity of So in cultured cells and to promote eye formation in Drosophila. Using heterologous leucine zipper domains, we specifically reconstituted the So{Delta}Eya-Eya PPI and show that this complex is transcriptionally active in cells and can rescue eye development. PPI-Rescue was also used to restore transcriptional activity to So{Delta}PPI (V111E), an allele that mimics the human SIX1(V17E) allele associated with Branchio-Oto-Renal syndrome. PPI-Rescue thus represents an innovative approach to understanding the complex molecular logic of transcription complexes in both development and disease.

developmental biology↗

Neural Crest-Derived Endocardial Cells Required for Heart Valve Development

Abnormalities in cardiac valves, which maintain unidirectional blood flow through the heart, affect 2-3% of people worldwide and are the most common form of structural heart disease (1).Yet the cell types that make up the valve, and how they communicate to direct development and homeostasis, remain poorly understood. Here, we identify a rare, essential population of highly secretory valve endocardial cells in mouse and human that derive from migrating neural crest cells. Ablation of these cells in mice caused perinatal lethality with thickened leaflets, stenosis, and regurgitation, mirroring human valve disease. This subset of endocardial cells uniquely expresses the secreted signaling protein parathyroid hormone-like hormone (Pthlh). Global disruption of Pthlh caused valve stenosis and lethality and neural crest-specific deletion produced similar valve disease, with impaired maturation of valvular interstitial cells and disrupted bone morphogenetic protein signaling. These findings identify a previously unrecognized cell type and signaling pathway essential for valve morphogenesis, with implications for the pathogenesis and treatment of human valve defects.

developmental biology↗

Oocyte-stored Mif promotes preimplantation development as an embryonic extracellular signal

Mammalian preimplantation embryos develop more efficiently in groups than in isolation, suggesting that embryos secrete embryotrophic factors that promote development. However, the endogenous embryotrophic signals responsible for this long-recognized phenomenon remain incompletely defined. Using an unbiased proteomic screen for stable maternal proteins that may function as embryonic extracellular signals, we identified the cytokine macrophage migration inhibitory factor (Mif) as an abundant oocyte-stored protein that persists for several days after fertilization in mice. Quantitative measurements of spent culture medium reveal that developing embryos release Mif, with a substantial fraction derived from the maternal deposit. Extracellular Mif levels peak 3-4 days post fertilization, the same period when Mif knockout preimplantation embryos produce its strongest phenotype. Embryos lacking maternal, but not zygotic, Mif display defective blastocyst growth even in group culture. Individually cultured embryos exhibit similar blastocyst growth defects that can be rescued by supplementing recombinant Mif at physiologically relevant concentrations. Mif activates the PI3K-Akt-mTORC1 pathway through the cell-surface receptor Cd74 to promote blastocyst growth and cell proliferation. Together, these findings identify Mif as a potential endogenous contributor to the density-dependent embryotrophic effects and reveal that maternally stored proteins may function long after fertilization as extracellular signaling molecules to support preimplantation development in mammals.

developmental biology↗