Fig. 4

Huang et al., 2008 - Mypt1-mediated spatial positioning of Bmp2-producing cells is essential for liver organogenesis
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Fig. 4

Loss-of-function of the myosin phosphatase complex causes a liverless phenotype and the mypt1sq181 mutation impairs the formation of the myosin phosphatase complex by compromising the binding of Mypt1 to PP1c. (A) Genetic complementation test between hi2653 and sq181 (sq181 x hi2653). (B,C) Both mypt1-MO and PP1c-MO morphants were either liverless or exhibited a small liver (arrow). (D) FLAG-tagged zebrafish and mouse wild-type (w) and M36-mutant (m) Mypt11-305 were co-expressed with HA-tagged mouse PP1c in COS-7 cells, and were co-immunoprecipitated using an anti-FLAG antibody. PP1c was detected with an anti-HA antibody and Mypt1 with an antibody against human MYPT1 (PPP1R12A - HUGO). Cells transfected with HA-PP1c alone were used as the negative control (-); w, wild-type Mypt11-305; m, M36-Mypt11-305; zb, zebrafish; mus, mouse. (E) Immunofluorescence microscopy of Hela cells transfected with FLAG-tagged zebrafish wild-type Mypt11-305 (Mypt1) or mutant M36-Mypt11-305 (M36-Mypt1). Cells containing Mypt1 or M36-Mypt1 were detected with an anti-FLAG antibody (arrows) (left panels). Stress fibers were stained with TRITC-labeled phalloidin (right panels). Note that cells lacking Mypt1 or M36-Mypt1 (marked with *) contained significant amounts of stress fibers, as did cells transfected with M36-Mypt11-305 (arrows, lower right panel).

Expression Data
Knockdown Reagents:
Anatomical Term:
Stage: Protruding-mouth

Expression Detail
Antibody Labeling
Phenotype Data
Knockdown Reagents:
Observed In:
Stage: Protruding-mouth

Phenotype Detail
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