Fig. 5. The Notch pathway functions through activation of Su(H) to specify a pericardial cell fate in asymmetric lineages. A2-A7 hemisegments of stage 13 embryos were labeled with (A-D) Mef2 (green) and Eve (red), or (E-H) Eve only. (A,B) In numb mutants, the number of myocardial cells per hemisegment is reduced from six to four; the number of EPC is increased from two to an average of 3.6 per hemisegment; DA1 muscles are not formed. (C) Overexpression of numb in the mesodermal eve lineage (eme>numb) abolishes the formation of all EPCs and sometimes more than one DA1 muscle per hemisegments seems to be generated. (D) Overexpression of the eme>N(icd) either generate three or four EPCs per hemisegment, or abolish eve expression altogether. No DA1 muscle founders are formed, as judged by the absence of Eve and Mef2 double labeling. (E) Overexpression of eme-Su(H) does not seem to alter eve expression. (F) By contrast, eme>Su(H)vp16 exhibits a similar phenotype as eme-N(icd), in that no eve-expressing cells or only EPCs form in most segments. Occasionally, four EPCs as well as one forming DA1 muscle are observed, suggesting that these two cell types are specified independently (see text). (G) Overexpression of numb together with the N(icd) [eme>N(icd)+numb] in the mesodermal Eve lineage generates an intermediate phenotype. (H) By contrast, overexpression of numb together with Su(H)vp16 [eme>Su(H)vp16+numb] generates a phenotype that is indistinguishable from overexpression of Su(H)vp16 alone [eme>Su(H)vp16].

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