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Fig. 6. Model of endocrine subtype specification during pancreatic development. (A)
An endocrine precursor cell initially expresses both Arx and Pax4, most
probably in an inactive form. In a first round of competitive fate allocation,
an unknown factor determines which factor will predominate: if it is Arx, the
-cell fate will be specified (with Arx inhibiting Pax4
expression), whereas Pax4 will induce ß-/
-cell lineages through
the inhibition of Arx transcription (1). In the case of Pax4
prevalence, the resulting ß-/-cell precursor is poised to undergo
a second round of fate allocation (2). In this second event, Pax4 seemingly
induces the ß-cell fate at the expense of the -cell lineage. A
hypothetical `factor X' is envisioned to have an opposite function, promoting
the -cell fate to the detriment of ß-cell specification (3). (B-D)
Fate changes in the case of Arx (B), Pax4 (C), or combined
Arx/Pax4 (D) deficiency. See main text for details. For the purpose
of simplification, exocrine cell and PP-cell development are not
represented.
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