Fig. 9. Model of cardiac lineages, the effect of cell cycle arrest and the function of Numb-Notch in determining cardiac cell fates. (A) The Drosophila heart is from T3-A8 segments. Black lines indicate lineage relationships based on this study, Ward and Skeath (Ward and Skeath, 2000), and Alvarez et al. (Alvarez et al., 2003). (B) The effects of cell cycle arrest, numb mutants and double mutants of numb and CycA. (C) Block of cell divisions in A2-A7 abdominal segments are as indicated. Asymmetric segregation of Numb into one daughter cell, or blocking precursor division, promotes myocardial cell fate by inhibition of Notch signaling. By contrast, activation of Notch signaling or the absence of Numb causes the daughter cell, or undivided precursor, to adopt a non-myogenic pericardial cell fate. SMC, Svp myocardial cell; TMC, Tinman myocardial cell; SOPC, Svp-Odd pericardial cell; EPC Eve pericardial cell; TMLC, Tinman-Lbe myocardial cell; LPC, Lbe pericardial cell; OPC, Odd pericardial cell; DA1, dorsal acute muscle; DO2, dorsal oblique muscle 2; DA1sib; SSP, Svp-positive super progenitor; TSP, Tin-positive super progenitor. FEPC, FDO2, FDA1 and FDA1sib are founders of EPCs, DO2, DA1 and DA1sib, respectively. P2 and P15 are progenitors of the above founder cells.