Single-cell transcriptomics of human embryos has led to the identification of new genes enriched in the pluripotent epiblast (EPI). One transcription factor identified in these studies is KLF17, a zinc-finger protein from the Krüppel-like family of transcription factors. In this Issue, Rebecca Lea, Kathy Niakan and colleagues describe the role of KLF17 in acquisition of naïve pluripotency. They find that the expression pattern of KLF17 is largely coincident with that of the canonical pluripotency marker SOX2 throughout blastocyst development. Furthermore, KLF17 expression becomes restricted to presumptive EPI cells marked by SOX2 and NANOG in day seven post-fertilisation blastocysts, suggestive of a role for KLF17 in pluripotency regulation. Indeed, the authors demonstrate that ectopic expression of KLF17 is sufficient to reset primed human embryonic stem cells (hESCs) to a naïve pluripotent state when cultured in naïve permissive conditions. However, deletion of KLF17 using CRISPR/Cas9 gene editing reveals that KLF17 is not necessary for acquisition or maintenance of naïve pluripotency in vitro. Together, these data indicate a peripheral role for KLF17 in naïve hESC pluripotency, while its importance for pluripotency in the human embryo remains to be investigated.
Investigating the role of KLF17 in human pluripotency
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Investigating the role of KLF17 in human pluripotency. Development 15 November 2021; 148 (22): e148_e2201. doi:
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