Fig. 6

Knockout of sox1a and sox1b causes increase of V2b cells. (A-A″) Knockout of sox1aand sox1b increases gata2a⁺ cells in the V2 domain by 22%. (B-B″) tal1⁺ cells are increased by 83% in sox1a^−/−; sox1b^−/− embryos. (C-C″) Lack of sox1a/b results in an increase of tal2⁺ cells by 75%. (D-D″) The sox1a/b mutant has 35% more gata3⁺ cells. (E-E″) vsx2⁺ cells are not affected by the mutations. (F-F″) At 30 hpf, the gata3⁺ cells in the V2 domain are increased by 2.3-fold. (G-I) Double FISH of nkx1.2lb (red) and slc6a5 (green) at 30 hpf and quantification of nkx1.2lb⁺; slc6a5⁺ cells in I. Glycinergic nkx1.2lb⁺ cells were decreased by 22% in the mutant. Asterisks indicate double-labelled cells. Counts of gata2a⁺ cells (A-A″) were derived from the fourth somite to the tail on both spinal cord sides from five embryos. Counts of gata3-, tal2-, tal1-, vsx2- and nkx1.2lb; slc6a5-expressing cells were derived from the spinal cord above the yolk extension over five somites from three to eight embryos (B-F″). V2 cells, white arrowheads (A-F′). Wild-type (white) and mutant (black) values are presented as mean±s.e.m. in A″-F″,I from at least two independent experiments. Statistical significance was assessed using the unpaired two-tailed Student's t-test. *P≤0.05, **P≤0.01, ***P≤0.001. Lateral views at 24 hpf (A-E′) and 30 hpf (F-H″). Dorsal is upwards; anterior is leftwards. Scale bars: 25 µm.