FIGURE

Fig. 6

ID

ZDB-FIG-170224-12

Publication

Hamm et al., 2016 - Sema3d controls collective endothelial cell migration by distinct mechanisms via Nrp1 and PlxnD1

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Fig. 6

Loss of cell–cell contacts in the CCV leading edge did not depend on flow or Cdh5. (A) Antibody staining for ZO-1 and Cdh5 showed aberrant junction distribution and impaired cell shape upon sema3d loss. Arrowheads indicate gaps in Cdh5 protein distribution. (B) The length of Cdh5-positive cell–cell connections is reduced in sema3d morphants (n = 4). (C) Cell–cell connections in the CCV leading edge of cdh5^ubs8 mutant embryos are present, but the ECs exhibit holes inside the cells (pink arrowheads). (D) Flow inhibition with nifedipine and tricaine did not lead to lesions or impaired Actin cable alignment in the CCV leading edge. Parallel-arranged Actin cables are indicated by open arrowheads. (E) Quantification of cell–cell-contact length of CCV leading edge cells (n = 16). ***, P < 0.001; n.s., not significant. Error bars indicate SD.

Expression Data

Genes:	cdh5 EGFP
Antibodies:	Ab1-cdh5 Ab1-tjp1
Fish:	WT WT + MO2-sema3d mu240Tg cdh5^ubs8/ubs8; mu240Tg
Condition:	chemical treatment by environment: nifedipine
Knockdown Reagent:	MO2-sema3d
Anatomical Terms:	common cardinal vein bicellular tight junction common cardinal vein blood vessel endothelium common cardinal vein cell-cell junction
Stage:	Prim-15

Expression Detail

Antibody Labeling

Phenotype Data

Fish:	WT + MO2-sema3d mu240Tg cdh5^ubs8/ubs8; mu240Tg
Condition:	chemical treatment by environment: nifedipine
Knockdown Reagent:	MO2-sema3d
Observed In:	common cardinal vein blood vessel endothelial cell common cardinal vein cell-cell junction
Stage:	Prim-15

Phenotype Detail

Acknowledgments

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