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Lens placode planar cell polarity is dependent on Cdc42-mediated junctional contraction inhibition.

ABSTRACT: Development of the ocular lens commences with the formation of the lens placode, an epithelial structure that thickens and subsequently bends inward in a process called invagination. Invagination is observed during the development of many embryonic structures, but the spectrum of morphogenetic events driving this process are, in most cases, not fully understood. A characteristic commonly found in embryonic tissues undergoing epithelial reorganization is planar polarity, a property where cells are geometrically and/or molecularly orientated in a specific direction along the plane of an epithelium. Planar polarity is known to drive the morphogenesis of several epithelial structures, however its role during invagination events is less clear. We have found that at the onset of invagination, cells of the lens placode become geometrically planar polarized such that they are orientated toward a central point in the lens placode. Further investigation revealed that this is due to contraction of radially orientated junctions and the elongation of those circumferentially orientated. Radial junctions have an elevated localization of actomyosin and their contraction is dependent on the F-actin and Rho-kinase binding protein, Shroom3. Elongation of circumferential junctions is dependent upon Cdc42, a Rho-GTPase known to regulate polarity via the Par-complex. We determined that Cdc42 and members of the Par-complex inhibit Shroom3-induced contractility and promote anisotropic placode cell geometry through inhibition of junctional contraction. We postulate that invagination of the lens placode requires careful orchestration of these opposing processes which are mediated by the planar polarization of junctional proteins.

SUBMITTER: Muccioli M

PROVIDER: S-EPMC7370377 | biostudies-literature | 2016 Apr

REPOSITORIES: biostudies-literature

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Lens placode planar cell polarity is dependent on Cdc42-mediated junctional contraction inhibition.

Muccioli Maria M Qaisi Dalya D Herman Ken K Plageman Timothy F TF

Developmental biology 20160220 1

Development of the ocular lens commences with the formation of the lens placode, an epithelial structure that thickens and subsequently bends inward in a process called invagination. Invagination is observed during the development of many embryonic structures, but the spectrum of morphogenetic events driving this process are, in most cases, not fully understood. A characteristic commonly found in embryonic tissues undergoing epithelial reorganization is planar polarity, a property where cells ar ...[more]

PMID: 26902112

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Project description:Previous studies suggested that FGF signaling is important for lens formation. However, the times at which FGFs act to promote lens formation, the FGFs that are involved, the cells that secrete them and the mechanisms by which FGF signaling may promote lens formation are not known. We found that transcripts encoding several FGF ligands and the four classical FGF receptors are detectable in the lens-forming ectoderm at the time of lens induction. Conditional deletion of Fgfr1 and Fgfr2 from this tissue resulted in the formation of small lens rudiments that soon degenerated. Lens placodes lacking Fgfr1 and 2 were thinner than in wild-type embryos. Deletion of Fgfr2 increased cell death from the initiation of placode formation and concurrent deletion of Fgfr1 enhanced this phenotype. Fgfr1/2 conditional knockout placode cells expressed lower levels of proteins known to be regulated by FGF receptor signaling, but proteins known to be important for lens formation were present at normal levels in the remaining placode cells, including the transcription factors Pax6, Sox2 and FoxE3 and the lens-preferred protein ?A-crystallin. Previous studies identified a genetic interaction between BMP and FGF signaling in lens formation and conditional deletion of Bmpr1a caused increased cell death in the lens placode, resulting in the formation of smaller lenses. In the present study, conditional deletion of both Bmpr1a and Fgfr2 increased cell death beyond that seen in Fgfr2(CKO) placodes and prevented lens formation. These results suggest that the primary role of autocrine or paracrine FGF signaling is to provide essential survival signals to lens placode cells. Because apoptosis was already increased at the onset of placode formation in Fgfr1/2 conditional knockout placode cells, FGF signaling was functionally absent during the period of lens induction by the optic vesicle. Since the expression of proteins required for lens formation was not altered in the knockout placode cells, we can conclude that FGF signaling from the optic vesicle is not required for lens induction.

Dataset Information

Lens placode planar cell polarity is dependent on Cdc42-mediated junctional contraction inhibition.

Publications

Lens placode planar cell polarity is dependent on Cdc42-mediated junctional contraction inhibition.

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