Figure 3.

The turtle gene products act as netrin-independent midline attractants. (A) Df(1)NP-5 homozygous embryos are missing the netA and netB genes and, consequently, exhibit gaps in their longitudinal connectives (arrow) and fragmented commissures (arrowhead), as revealed by BP102 staining. (B, C) Df(1)NP-5; tutl^ex383/+ embryos show an enhancement of both defects (B, arrow and arrowhead), while Df(1)NP-5; tutl^ex383 double mutants have an extreme reduction in commissures, with only one thin fragmented commissure formed throughout the length of the embryo (C). (D) fra^GA957 homozygous embryos exhibit gaps in their longitudinal connectives (arrow) and fragmented commissures (arrowhead) as revealed by BP102 staining. (E)fra^GA957, tutl^ex383/+ embryos show an enhancement of both defects. while fra^GA957,tutl^ex383 double mutants have an extreme reduction in commissures (arrowhead) (G) slit¹/+, robo⁵/+ embryos have a reduction in slit signaling that can produce a minor midline crossing defect revealed by FasII staining (arrowhead). (H, I) slit¹/+, robo⁵/+, tutl^ex383/+ triple heterozygotes do not show any enhancement nor suppression of the FasII axon crossing defect compared to slit¹/+, robo⁵/+ double heterozygotes alone. (J) abl¹ homozygous embryos do not show any defect in commissure or longitudinal connectives as revealed by BP102 staining (arrow and arrowhead). (K, L) tutl^ex383; abl¹/+ embryos show an enhancement of commissural defects (K), while tutl^ex383; abl¹ double mutants have an extreme reduction in commissure formation (L, arrow) and fragmented longitudinal connectives (L, arrowhead).