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. 2009 Dec 15;136(24):4089–4098. doi: 10.1242/dev.040386

Fig. 4.

Fig. 4.

spdo potentiates Notch signaling in the absence of numb. Left and middle panels show lateral view; right panel shows dorsal view of eve expression in the mesoderm. (A-A″) In wild type, mesodermal Eve+ equivalence groups (arrows, A) generate Eve+ precursor cells (arrows, A′) that produce the EPCs (arrows, A″), and the Eve+ DA1 muscles (white arrows, A″). (B-B″) In numb mutant embryos, equivalence group formation and precursor selection occurs normally (arrows, B,B′); however, defects in asymmetric divisions lead to a doubling of EPC numbers (arrows, B″) and a loss of DA1 muscles (white arrows, B″). (C-C″) Eve+ equivalence groups form normally in numb mutant embryos that misexpress spdo in the mesoderm under the control of twist-GAL4 (arrows); however, Eve+ precursors fail to segregate from half of these groups (arrowhead, C′), resulting in fewer EPCs (arrows, C″). (D-D″) Eve+ equivalence groups form, albeit with reduced eve expression, upon mesodermal expression of a constitutively active form of Notch (NotchΔECN) in wild-type embryos; however, few precursors and EPCs arise in this background (arrows, D′,D″). Anterior, left.