Limits...
The Rho GTPase Cdc42 regulates hair cell planar polarity and cellular patterning in the developing cochlea.

Kirjavainen A, Laos M, Anttonen T, Pirvola U - Biol Open (2015)

Bottom Line: Atypical protein kinase C (aPKC), a putative Cdc42 effector, colocalized with Cdc42 at the hair cell apex, and aPKC expression was altered upon Cdc42 depletion.Our data suggest that Cdc42 together with aPKC is part of the machinery establishing hair cell planar polarity and that Cdc42 acts on polarity through the cell-surface microtubule network.In addition, our data demonstrates that Cdc42 is required for stereociliogenesis in the immature cochlea.

View Article: PubMed Central - PubMed

Affiliation: Department of Biosciences, Viikinkaari 1, 00014 University of Helsinki, Finland.

No MeSH data available.


Related in: MedlinePlus

Cellular disorganization, but unaltered expression of adhesion proteins in the organ of Corti of Cdc42loxP/loxP;Fgfr3-iCre-ERT2 mice at E18.5.(A,B) Phalloidin labeling shows the organization of OHCs into three rows in the control specimen. In the organ of Corti of the mutant mouse, misplacement of some OHCs in between the rows is seen. The organization of the row of unrecombined IHCs is unaltered. Both views are from the medial coil. (C–D′) Confocal views at the level of adherens junctions show comparable expression of β-catenin (C,D) and E-cadherin (C′,D′) in the two genotypes. Arrows in D point to atypical intercellular contacts. (E,F) Nectin 3 immunofluorescence is comparable in the contact sites between OHCs and Deiters' cells in both genotypes. Abbreviations: IHC, inner hair cell; OHC, outer hair cell; β-cat, β-catenin; E-cad, E-cadherin. Scale bar shown in F: A,B, 6 µm; C–F, 5 µm.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
getmorefigures.php?uid=PMC4400594&req=5

f03: Cellular disorganization, but unaltered expression of adhesion proteins in the organ of Corti of Cdc42loxP/loxP;Fgfr3-iCre-ERT2 mice at E18.5.(A,B) Phalloidin labeling shows the organization of OHCs into three rows in the control specimen. In the organ of Corti of the mutant mouse, misplacement of some OHCs in between the rows is seen. The organization of the row of unrecombined IHCs is unaltered. Both views are from the medial coil. (C–D′) Confocal views at the level of adherens junctions show comparable expression of β-catenin (C,D) and E-cadherin (C′,D′) in the two genotypes. Arrows in D point to atypical intercellular contacts. (E,F) Nectin 3 immunofluorescence is comparable in the contact sites between OHCs and Deiters' cells in both genotypes. Abbreviations: IHC, inner hair cell; OHC, outer hair cell; β-cat, β-catenin; E-cad, E-cadherin. Scale bar shown in F: A,B, 6 µm; C–F, 5 µm.

Mentions: To study the possible involvement of Cdc42 in cellular patterning in the OC, whole mount specimens were labeled with phalloidin, marking F-actin. Cochlear specimens from control mice at E18.5 displayed precisely aligned hair cell rows, separated by supporting cell rows (Fig. 3A). In contrast, cochleas of the Cdc42 mutant mice showed occasional misplacement of OHCs between the cell rows, creating direct contacts between OHCs, as opposed to normal OHC patterning with intervening supporting cells (Fig. 3B). These defects were seen in the medial coil of the cochlea and were mostly absent in the basal and apical coils. The unrecombined IHCs were properly aligned along the length of the cochlear duct of the mutant mice (Fig. 3A,B).


The Rho GTPase Cdc42 regulates hair cell planar polarity and cellular patterning in the developing cochlea.

Kirjavainen A, Laos M, Anttonen T, Pirvola U - Biol Open (2015)

Cellular disorganization, but unaltered expression of adhesion proteins in the organ of Corti of Cdc42loxP/loxP;Fgfr3-iCre-ERT2 mice at E18.5.(A,B) Phalloidin labeling shows the organization of OHCs into three rows in the control specimen. In the organ of Corti of the mutant mouse, misplacement of some OHCs in between the rows is seen. The organization of the row of unrecombined IHCs is unaltered. Both views are from the medial coil. (C–D′) Confocal views at the level of adherens junctions show comparable expression of β-catenin (C,D) and E-cadherin (C′,D′) in the two genotypes. Arrows in D point to atypical intercellular contacts. (E,F) Nectin 3 immunofluorescence is comparable in the contact sites between OHCs and Deiters' cells in both genotypes. Abbreviations: IHC, inner hair cell; OHC, outer hair cell; β-cat, β-catenin; E-cad, E-cadherin. Scale bar shown in F: A,B, 6 µm; C–F, 5 µm.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4400594&req=5

f03: Cellular disorganization, but unaltered expression of adhesion proteins in the organ of Corti of Cdc42loxP/loxP;Fgfr3-iCre-ERT2 mice at E18.5.(A,B) Phalloidin labeling shows the organization of OHCs into three rows in the control specimen. In the organ of Corti of the mutant mouse, misplacement of some OHCs in between the rows is seen. The organization of the row of unrecombined IHCs is unaltered. Both views are from the medial coil. (C–D′) Confocal views at the level of adherens junctions show comparable expression of β-catenin (C,D) and E-cadherin (C′,D′) in the two genotypes. Arrows in D point to atypical intercellular contacts. (E,F) Nectin 3 immunofluorescence is comparable in the contact sites between OHCs and Deiters' cells in both genotypes. Abbreviations: IHC, inner hair cell; OHC, outer hair cell; β-cat, β-catenin; E-cad, E-cadherin. Scale bar shown in F: A,B, 6 µm; C–F, 5 µm.
Mentions: To study the possible involvement of Cdc42 in cellular patterning in the OC, whole mount specimens were labeled with phalloidin, marking F-actin. Cochlear specimens from control mice at E18.5 displayed precisely aligned hair cell rows, separated by supporting cell rows (Fig. 3A). In contrast, cochleas of the Cdc42 mutant mice showed occasional misplacement of OHCs between the cell rows, creating direct contacts between OHCs, as opposed to normal OHC patterning with intervening supporting cells (Fig. 3B). These defects were seen in the medial coil of the cochlea and were mostly absent in the basal and apical coils. The unrecombined IHCs were properly aligned along the length of the cochlear duct of the mutant mice (Fig. 3A,B).

Bottom Line: Atypical protein kinase C (aPKC), a putative Cdc42 effector, colocalized with Cdc42 at the hair cell apex, and aPKC expression was altered upon Cdc42 depletion.Our data suggest that Cdc42 together with aPKC is part of the machinery establishing hair cell planar polarity and that Cdc42 acts on polarity through the cell-surface microtubule network.In addition, our data demonstrates that Cdc42 is required for stereociliogenesis in the immature cochlea.

View Article: PubMed Central - PubMed

Affiliation: Department of Biosciences, Viikinkaari 1, 00014 University of Helsinki, Finland.

No MeSH data available.


Related in: MedlinePlus