We find Azot expression in a wide range of ‘‘less fit’’ cells, such
as WT cells challenged by the presence of ‘‘supercompetitors,’’
slow proliferating cells confronted with normal proliferating cells,
cells with mutations in several signaling pathways (i.e., Wingless,
JAK/STAT, Dpp), or photoreceptor neurons forming incomplete
ommatidia. In order to be expressed specifically in ‘‘less fit’’
cells, the transcriptional regulation of azot integrates fitness information
from at least three levels: (1) the cell’s own levels of
FlowerLose isoforms, (2) the levels of Sparc, and (3) the levels of
Lose isoforms in neighboring cells. Therefore, Azot ON/OFF
regulation acts as a cell-fitness checkpoint deciding which viable
cells are eliminated. We propose that by implementing a cell-
fitness checkpoint, multicellular communities became more
robust and less sensitive to several mutations that create viable
but potentially harmful cells. Moreover, azot is not involved in
other types of apoptosis, suggesting a dedicated function,
and—given the evolutionary conservation of Azot—pointing to
the existence of central cell selection pathways in multicellular
animals