Spalt (sal)-like proteins are transcription factors that are described for nematodes, shrimp, insects and multiple chordata analyzed till date.
Mutations in genes of the spalt like transcription factor family have been shown to manifest in phenotypic aberrations in several model organisms. Moreover, humans carrying mutations in spalt like genes suffer from various developmental defects.
A deeper understanding of the role of Sall genes in mammalian development will therefore be required to gain insights into general development as well as elucidate the underlying principles of Townes-Brocks Syndrome and Duane-Radial Ray Syndrome, caused by mutations in SALL1 and SALL4 respectively. Mouse is the closest system to humans that is accessible to reverse genetics. Therefore, I decided to study the effects of loss of Sall orthologous genes in Mus musculus by means of genetic manipulation.
This approach generated phenotypes with full penetrance that enables the investigation of cellular responses to SALL proteins. As a result, I have identified a novel function for Sall genes in maintenance of pluripotency within progenitor populations
