Transcription factor implicated in the cell fate determination in various organs. Binds to the E-box consensus sequence 5'-CANNTG-3'. Plays a role in early and late pancreas development and differentiation. Important for determining whether cells allocated to the pancreatic buds continue towards pancreatic organogenesis or revert back to duodenal fates. May be involved in the maintenance of exocrine pancreas-specific gene expression including ELA1 and amylase. Required for the formation of pancreatic acinar and ductal cells. Plays an important role in cerebellar development. Directly regulated by FOXN4 and RORC during retinal development, FOXN4-PTF1A pathway plays a central role in directing the differentiation of retinal progenitors towards horizontal and amacrine fates. Component of the pancreas transcription factor 1 complex (PTF1) which is composed of TCF3/p75, TCF12/p64 and PTF1A/p48. TCF3 is responsible for the nuclear import of the p48/p64 complex. Interacts with TCF3 and RBPSUH/RBP-Jkappa. In the cytoplasm loses its ability to form the PTF1 complex. Expressed in precursors of pancreatic islets, acini and ducts. Expressed at an early stage of pancreas development, shortly after the onset of endodermal budding that forms the pancreatic anlage. In 9.5 dpc embryo, expression is in the myelencephalon and the neural tube at the cervical level. In the 10.5 dpc embryo expression expands as a thin stripe to the posterior end of the neural tube. The central nervous system anterior to the myelencephalon is devoid of expression at this stage. In 12-12.5 dpc embryo, expression expands anteriorly to the cerebellum region. During retinogenesis, restricted to postmitotic neuronal precursor population in the ventricular zone of the developing retina. Not expressed before 12.5 dpc when is detected in the central region of the retina. By 14.5, expands from the center to the entire retina. Between 16.5 dpc and P1, continues to be expressed strongly in a subset of cells within the outer neuroblastic layer. Expression begins to be down-regulated by P2 and is undetectable in retinas from P6. Early postnatal lethal phenotype characterized by a lack of the exocrine pancreas, however, islet-like endocrine cell clusters are formed. A redirection of pancreatic precursors to intestinal fates is seen. At 16.5 dpc embryos show reduced size of cerebellar primordium and cerebellar aplasia.