Imprecise excision of the P{EPgy2}SdcEY04602 insertion, resulting in a 5.8kb deletion that removes the complete open reading frame of Sara and a portion of the Sdc gene.
Sara12 escapers exhibit a midgut phenotype at 15 days after hatching. Midgut length is significantly reduced in homozygous Sara12 and Sara12/Df(2R)48 mutants with respect to wild type. The mitotic index is also decreased by half and the number of intestinal stem cells (ISCs) in the posterior midgut 15 days after hatching is significantly increased compared with wild type. Fewer Sara12 mutant clones are recovered in the adult posterior midgut than in wild type, and the clones that are recovered contain fewer cells. A higher proportion of ISC symmetric divisions occur compared to wild type. The number of enterocytes is increased at the expense of enteroendocrine cells in Sara12 mutant clones.
Sara12/Df(2R)PK1 third larval instar wing discs show an increase in the level of apoptosis compared to wild type.
9.4% of Sara12 embryos lacking both maternal and zygotic Sara+ function die as embryos with cellularization defects, 34.4% die as embryos without a gross morphological phenotype, while 56.3% survive to form mobile first instar larvae.
Zygotic Sara12 mutants die during late larval and pupal development. 5% of these homozygotes survive to adulthood, showing variable vein defects, such as delta formation at the junctions with the margin, branching of the posterior crossvein and partial vein duplications.
92.2% of Sara12 mutants lacking both maternal and zygotic Sara+ function die during embryogenesis, with various phenotypes including cellularization and dorsal/ventral patterning defects.
Targeting of endosomes to the central spindle is normal in dividing wing disc cells in Sara12 zygotic mutants.
Sara12/Df(2R)PK1 wing discs show an increase in the level of apoptosis compared to wild type.
Sara12 is partially rescued by SaraUbi.GFP
Expression of SaraUbi.T:Avic\GFP largely rescues the lethality associated with homozygous Sara12.
