In mammals, however, Mib1 is essential for Notch-mediated cell fate decisions in all contexts of mammalian development examined in this study and the previous studies [13].
This provides the first genetic evidence that Mib1 is required for the Notch-mediated cell fate decisions in a single organism, especially in mammals.
In Drosophila, both Notch ligands, Delta and Serrate, require an E3 ubiquitin ligase, either dMib or dNeur, for their activity in Notch-mediated cell fate decisions dependent on expression patterns [10] [12].
Then its interaction with transcription factors results in the regulation of target genes mediating cell fate, proliferation, and migration.
Transcription factors are usually classified into different families based on their sequence of functional DNA-binding or protein-binding domains, which are highly conserved among many species and include many members mediating cell fate allocation during animal and plant development [ 1– 11].
The potential of PAX7 to mediate cell-fate decisions in the pituitary gland is related to its chromatin-remodelling role and indicates that differentiation mechanisms are analogous in different tissues (Budry et al, 2011).
In fact, ubc-25 was previously recognized for roles not directly related to the cell cycle, such as promoting a Ras-mediated cell-fate decision (Rocheleau et al. 2008) and maintaining neuromuscular homeostasis (Schulze et al. 2003).
In light of this functional analogy between c-Abl and p53, it is possible that c-Abl could also act in the form of a molecular switch, mediating cell-fate decisions and inducing a shift from prosurvival to pro-death mechanisms under the appropriate circumstances.
