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#MST1/2

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Fertilization in mammals-lll

MST1/2 and LATS1/2 signaling influences:

During mammalian preimplantation development Hippo pathway components MST1/2 and LATS1/2 regulate formation and patterning of blastula equivalent blastocyst. In inner apolar blastomeres active Hippo cascade phosphorylates LATS1/2 via MST1/2, leading to phosphorylated YAP cytoplasmic retention and inner cell mass fate. In outer polar cells Hippo off allows nuclear YAP-TEAD interaction inducing Cdx2-driven trophectoderm fate and blastocoel cavitation. Loss of MST/LATS disrupts outside-inside lineage allocation yielding defective blastocysts. These kinases are not involved in capacitation, acroso

Ref: Cockburn et al., Developmental Cell 2013: Hippo pathway MST1/2 LATS1/2 positioning trophectoderm versus inner cell mass.

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Fertilization in mammals-iv

MST1/2, LATS1/2 pathways influence:

MST1/2 and LATS1/2 are core kinases of Hippo signaling pathway controlling first lineage decisions during morula-to-blastocyst transition. In inner apolar cells Hippo is active: MST1/2 phosphorylate LATS1/2 which phosphorylate YAP, sequestering it cytoplasmically and permitting Nanog, Oct4 expression for inner cell mass fate. In outer polar cells Hippo is off, unphosphorylated YAP translocates to nucleus, interacts with TEAD4 to induce Cdx2 and Gata3 driving trophectoderm differentiation and blastocoel formation. Thus pathway does not regulate acrosome or capacitation but blastocyst patterning

Ref: Korotkevich et al., Dev Cell 2017 & Nishioka et al., Dev Cell 2009: Hippo MST1/2 LATS1/2 YAP regulation of blastocyst trophectoderm.

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