Abstract
Kruppel-like factor 4 (Klf4) is a zinc finger transcription factor and plays crucial roles in Xenopus embryogenesis. However, its regulation during embryogenesis is still unclear. Here, we report that Tcf7l1, a key downstream transducer of the Wnt signaling pathway, could promote Klf4 transcription and stimulate Klf4 promoter activity in early Xenopus embryos. Furthermore, cycloheximide treatment showed a direct effect on Klf4 transcription facilitated by Tcf7l1. Moreover, the dominant negative form of Tcf7l1 (dnTcf7l1), which lacks N-terminus of the β-catenin binding motif, could still activate Klf4 transcription, suggesting that this regulation is Wnt/β-catenin independent. Taken together, our results demonstrate that Tcf7l1 lies upstream of Klf4 to maintain its expression level during Xenopus embryogenesis.
Highlights
Kruppel-like factor 4 (Klf4), a zinc finger containing transcription factor of the Kruppel-like factor family, plays critical roles in stem cell biology and early embryogenesis
The expression level of Klf4 was very low in uninjected control embryos, while Klf4 transcription level was dramatically upregulated in the animal pole and the lateral region in embryos injected with Tcf7l1 mRNA (Fig. 1A, C)
Our results showed that Tcf7l1 dramatically activated Klf4 transcription
Summary
A zinc finger containing transcription factor of the Kruppel-like factor family, plays critical roles in stem cell biology and early embryogenesis. Knockdown of Klf results in the differentiation of ES cells[3–4]. During Xenopus embryogenesis, Klf is expressed maternally and zygotically[5], which is vital for germ layer formation and body axis patterning. Due to its important functions in cell fate determination in both ES cells and early embryos, Klf should be maintained at a correct level so that cell differentiation could continue properly. A few attempts so far have been done on the transcription regulation mechanism of Klf in ES cells, some cancer cells and adult cells[7–9]. Besides the mechanism described above, Klf could upregulate its own transcription by binding to its promoter[1,18]. The previous studies have provided some clues of the regulation mechanism of Klf, there is still
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