Errata for vol. 12, p. 304

The fate of the progeny from P2, P15, and P17 progenitors in wild-type, insc^P49, andnumb³ embryos. Embryos were double stained for Eve (red) and Kr (green). Stage 12 (A–F′) and stage 14 (G–I) wild-type (A,G), insc^P49(B–D,H), and nb³(E–F′,I) embryos are shown. (A) Three consecutive wild-type hemisegments at mid- to late-stage 12. At this stage, the two EPC (red) are already present. The Kr⁺Eve⁺ FDA1 (yellow) and the Kr⁺ FDO1 (green) are also evident. (B–D) In insc^P49embryos, the incomplete expressivity of the mutant phenotype is evident in different hemisegments and is characterized by duplication of FDO1 (B), loss of the two EPC (C,*), and duplication of the FDA1 (D). (E–F′) The opposite phenotype is found in nb³ embryos: Two FEPCs are detected at early stage 12, which are enlarging to divide (E), and no putative FDA1 and FDO1 are detected that express Eve and/or Kr. At mid-stage 12, extra EPCs are detected (F’). (F,F′) Two different focal planes of the same mutant hemisegment at mid-stage 12. (F) The FDA1 (yellow cells) is losing Eve and Kr expression; likewise, Kr expression is decaying in both siblings produced by division of P17 (arrows). (G) The characteristic pattern of EPC and precursors of DA1 and DO1 in a wild-type embryo at stage 14. (H) In aninsc^P49 embryo, loss of EPC (*) and duplication of the precursors of muscles DA1 (yellow syncytia, arrows) and DO1 (green syncytia, arrows) are evident. (I) The opposite phenotype is observed in a nb³ embryo; extra EPCs and the absence of DA1 and DO1 muscle precursors.