SIP1 mediates cell-fate decisions between neuroectoderm and mesendoderm in human pluripotent stem cells (Cell Stem Cell, 2010, 6(1):59-70)

報告日期: 2010/05/25
報告時間: 17:10/18:00
報告學生: 呂姿誼
講評老師: 謝清河



SIP1 Mediates Cell-Fate Decisions between Neuroectoderm and Mesendoderm in Human Pluripotent Stem Cells

Cell Stem Cell 6, 59–70, January 8, 2010


Speaker: Tzu-Yi Lu

Commentator: Patrick C.H. Hsieh

Time: 17:10-18:00, 2010/05/25

Room: 602


This study used different culture medium and gene transferring technique to understand the underlying cell-fate decisions between neuroectoderm and mesendoderm in human embryonic stem cells (hESCs). Activin-Nodal signaling was known to maintain hESCs pluripotency and also to induce mesendoderm differentiation. The thesis behind those contradictory functions was not clear. The novelty of this article was to demonstrate that the expression of the germ layer differentiation could correlate with each other by activating or repressing Smad-interacting protein 1 (SIP1). SIP1 could enhance neuroectoderm differentiation and blocks BMP-induced mesendoderm fates at the same time. SIP1 could prevent Activin-Nodal signaling from driving pluriopotent hESCs into mesendoderm. Higher levels of SIP1 expression favors neuroectoderm differentiation and lower level appears to maintain pluriopotency. Mouse epiblast stem cells seems to have similar culture results, implying SIP1 expression could be conserved in mammalian development. Overall, this paper reveal that SIP1 regulate the cell-fate decision between neuroectoderm and mesendoderm in the progression from pluripotency to primary germ layer differentiation.