AI Article Synopsis
- TFCP2L1 is a key transcription factor important for keeping mouse embryonic stem cells (mESCs) in a pluripotent, undifferentiated state.
- Research shows that reducing TFCP2L1 leads to the expression of markers for different cell types, indicating a shift from pluripotency.
- The study also identifies the specific regions in TFCP2L1 that are essential for maintaining this undifferentiated state and highlights the role of MTA1 in supporting TFCP2L1's function.
Article Abstract
TFCP2L1 is a transcription factor that is crucial for self-renewal of mouse embryonic stem cells (mESCs). How TFCP2L1 maintains the pluripotent state of mESCs, however, remains unknown. Here, we show that knockdown of in mESCs induces the expression of endoderm, mesoderm and trophectoderm markers. Functional analysis of mutant forms of TFCP2L1 revealed that TFCP2L1 depends on its N-terminus and CP2-like domain to maintain the undifferentiated state of mESCs. The N-terminus of TFCP2L1 is mainly associated with the suppression of mesoderm and trophectoderm differentiation, while the CP2-like domain is closely related to the suppression of endoderm commitment. Further studies showed that MTA1 directly interacts with TFCP2L1 and is indispensable for the TFCP2L1-mediated self-renewal-promoting effect and endoderm-inhibiting action. TFCP2L1-mediated suppression of mesoderm and trophectoderm differentiation, however, seems to be due to downregulation of expression. Our study thus provides an expanded understanding of the function of TFCP2L1 and the pluripotency regulation network of ESCs.
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| http://dx.doi.org/10.1242/jcs.206532 | DOI Listing |
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