ZFIN Image: Gokey et al., 2015, Fig. 4

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Fig. 4

Inhibiting V-ATPase function disrupted cardiac left–right asymmetry, KV organ size and KV cilia formation. (A) Concanamycin A treatments between the 50% epiboly stage and the 6 somite stage or MO depletion of Atp6v1f altered heart looping as compared to controls. Heart defects in atp6v1f MO embryos were significantly rescued by atp6v1f mRNA. (B–D) Immunofluorescent staining of KV using aPKC and acetylated-Tubulin markers. (E–G) Quantification of KV cilia length (E), cilia number (F), and KV size (G) in DMSO control (n=17) embryos, concanamycin A treated (n=26) embryos and atp6v1f MO injected (n=22) embryos. Scale bars=5 µm.

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Acknowledgments

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Reprinted from Developmental Biology, 407(1), Gokey, J.J., Dasgupta, A., Amack, J.D., The V-ATPase accessory protein Atp6ap1b mediates dorsal forerunner cell proliferation and left-right asymmetry in zebrafish, 115-30, Copyright (2015) with permission from Elsevier. Full text @ Dev. Biol.