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Evolutionary modification of AGS protein contributes to formation of micromeres in sea urchins
Evolutionary modification of AGS protein contributes to formation of micromeres in sea urchins
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Evolutionary modification of AGS protein contributes to formation of micromeres in sea urchins
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Evolutionary modification of AGS protein contributes to formation of micromeres in sea urchins
Evolutionary modification of AGS protein contributes to formation of micromeres in sea urchins

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Evolutionary modification of AGS protein contributes to formation of micromeres in sea urchins
Evolutionary modification of AGS protein contributes to formation of micromeres in sea urchins
Journal Article

Evolutionary modification of AGS protein contributes to formation of micromeres in sea urchins

2019
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Overview
Evolution is proposed to result, in part, from acquisition of new developmental programs. One such example is the appearance of the micromeres in a sea urchin that form by an asymmetric cell division at the 4 th embryonic cleavage and function as a major signaling center in the embryo. Micromeres are not present in other echinoderms and thus are  considered as a derived feature, yet its acquisition mechanism is unknown. Here, we report that the polarity factor AGS and its associated proteins are responsible for micromere formation. Evolutionary modifications of AGS protein seem to have provided the cortical recruitment and binding of AGS to the vegetal cortex, contributing to formation of micromeres in the sea urchins. Indeed, introduction of sea urchin AGS into the sea star embryo induces asymmetric cell divisions, suggesting that the molecular evolution of AGS protein is key in the transition of echinoderms to micromere formation and the current developmental style of sea urchins not seen in other echinoderms. Micromeres in a sea urchin embryo are formed by asymetric cleavage but what molecular mechanisms regulate their formation is unclear. Here, the authors show that sea urchins modify an evolutionarily conserved AGS-dependent mechanism to induce asymmetric cell divisions in the early embryo.