Utf1, or Undifferentiated embryonic cell transcription factor 1, is a proline-rich, nuclear protein. It is highly conserved among placental mammals and prominently expressed in pluripotent, germ, and cancer cells. In pluripotent and germ cells, it is implicated in proper cell differentiation. Functionally, it aids in establishing a favorable chromatin state in embryonic stem cells, reducing “transcriptional noise” [1].

In Utf1 null embryos, proper development almost entirely depends on the presence of functional Utf1 alleles in the parental germline, indicating a link between its in-vitro epigenetic role in ESC pluripotency and intergenerational epigenetic inheritance in vivo [2]. In human iPSCs, Utf1 knockout resulted in significantly reduced reprogramming efficiency and increased spontaneous differentiation, highlighting its crucial role in maintaining human iPSC identity and stability [3]. In P19 embryonal carcinoma cells, UTF1-deficiency promoted retinoic acid-induced neuronal differentiation [4]. In male fertility, UTF1 is crucial for spermatogenesis and maintaining male fertility in mice, and is expressed in undifferentiated spermatogonia in stallions [1,5].

In conclusion, Utf1 is essential for processes such as cell differentiation, pluripotency maintenance, germ cell development, and spermatogenesis. Gene knockout models, especially in mice, have been crucial in revealing these functions. Its role in cancer shows tissue-specific function as either an oncogene or a tumor suppressor, highlighting the importance of further research on Utf1 in understanding disease mechanisms [1].