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  current news   Press   selected story    
     
  4th November  
 

Mypt1-Mediated Spatial Positioning of Bmp2-Producing Cells Is Essential for Liver Organogenesis

 
 




Abstract
Mesodermal tissues produce various inductive signals essential for morphogenesis of endodermal organs. However, little is known about how the spatial relationship between the mesodermal signal-producing cells and their target endodermal organs is established during morphogenesis. Here we report that a mutation in the zebrafish myosin phosphatase targeting subunit 1 (mypt1) causes abnormal bundling of actin filaments and disorganization of lateral plate mesoderm (LPM) cells. As a result, the coordination between mesoderm and endoderm cell movements is disrupted. Consequently, the two stripes of Bmp2a-expressing cells in the LPM fail to align in a V-shaped pocket sandwiching the liver primordium. Mispositioning Bmp2a producing cells with respect to the liver primordium leads to a reduction of hepatoblast proliferation and final abortion of hepatoblasts by apoptosis that causes the liverless phenotype. Our results demonstrate that Mypt1 mediates coordination between mesoderm and endoderm cell movements in order to carefully position the liver primordium such that it receives a Bmp signal that is essential for liver formation in zebrafish.

 
 


 
 


Figure Legend: The mypt1sq181 mutation alters actin assembly in LPM and endoderm cells.

(A,B) Cross-sections from wild-type (WT) and mutant (mu) zebrafish embryos in the Tg(gutGFP)S584 background (green) stained with phalloidin (red). (C-F) High-magnification views of boxed regions in A (C,D) and B (E,F) showing abnormal aggregations of actin filaments (arrows) and cell organization in the mutant endoderm (C versus E) and LPM (D versus F) cells.

For more information on Jin Rong PENG’s Lab, Please Click here.