Figure 7 - Summary Diagrams of the Neuromeric Organization
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(A) Wild type. otd is expressed in most parts of the neuromere b1 except for the most anterior region. It also is expressed in the posterior compartments of neuromere b2 and b3 with little overlapping with ems, which is expressed in the anterior compartments of neuromeres b2 and b3. bsh is expressed in three clusters in the b1 neuromere. ey is expressed in several domains in the b1 neuromere and in the posterior compartments of the b2 and b3 neuromeres with little overlap with ems. otd, ems and ey also are expressed in the subesophageal ganglia and VNC (broken lines). Expression patterns of the anterior HOM-C genes, lab, Dfd and Scr, also are indicated. The exd and hth genes are coexpressed in all the neuromeres. Small red circles, en cells; ol, optic lobe primordia.
(B) Maternal and zygotic exd null mutant or hth null mutant. Mutations in exd or hth result in profound defects in axogenesis and regional patterning of the embryonic brain. The axonal scaffolds are completely disrupted and the brain commissure is shifted posteriorly (in neuraxis). The supra- and subesophageal ganglia remain separated. Optic lobes are residual. Subesophageal neuromeres are severely affected or missing. Molecularly, expression of otd is significantly stimulated in most parts of the brain. Expression of the ems and HOM-C genes are suppressed. Expression of ey also is suppressed in most parts of the brain except for the anterior terminal region. In addition, en expression in en-b1 is up regulated recruiting additional cells. Expression of bsh is not only stimulated in the b1 neuromere, but also ectopically induced in neuromere b2.
|Flybrain Development Patterning Defects Figure 7|
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