PgmNr Z541: Myo1D, an unconventional myosin regulates kupffer’s vesicle lumenogenesis in zebrafish.

Authors:
M. Saydmohammed; H. Yagi; T. Feinstein; D. Kostka; CW Lo; M. Tsang


Institutes
University of Pittsburgh, Pittsburgh, PA.


Abstract:

During zebrafish development, a transient ciliated organ known as the kupffer vesicle (KV) forms and contributes to establishing laterality in the embryo. The activity of motile cilia in the KV results in asymmetric flow of extra embryonic fluid and contributes to the left-right arrangement of visceral organs. The molecular mechanisms that contribute to the formation of KV lumen still remain elusive. Recent work in Drosophila has identified a novel situs inversus gene encoding unconventional type 1D Myosin (myo1D).  Here, we show that zebrafish myo1D is essential for KV lumenogenesis. Targeted mutation in the myo1D gene by TALENs affected the formation of KV lumen and randomized heart and gut looping. Confocal imaging of the KV formation revealed failure of the KV lumen to expand.   Disrupted KV lumenogenesis in myo1D mutants was due to mislocalization of E cadherin and β-catenin that resulted in loss of apical basal polarity in cells that form the KV. myo1D is expressed maternally and only the maternal-zygotic (MZ) mutant showed defective KV formation. Defective KV lumenogenesis phenotype was recapitulated by injecting with antisense morpholino (MO) targeting the myo1D gene. In summary, myo1D is one of the earliest unconventional myosin motors expressed in zebrafish that regulate KV lumenogenesis and critical for proper left right patterning in a vertebrate.



ZFIN Genetics Index
1. myo1D