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조익현,한평림,이강우,Hye-Yeong Ha 생화학분자생물학회 2011 Experimental and molecular medicine Vol.43 No.8
We previously reported that mice lacking JSAP1(jsap1-/-) were lethal and the brain of jsap1-/- at E18.5 exhibited multiple types of developmental defects, which included impaired axon projection of the corpus callosum and anterior commissures. In the current study,we examined whether the early telencephalic commissures were formed abnormally from the beginning of initial development or whether they arose normally, but have been progressively lost their maintenance in the absence of JSAP1. The early corpus callosum in the brain of jsap1+/+ at E15.5-E16.5 was found to cross the midline with forming a distinct U-shaped tract, whereas the early axonal tract in jsap1-/- appeared to cross the midline in a diffuse manner, but the lately arriving axons did not cross the midline. In the brain of jsap1-/- at E17.5, the axon terminals of lately arriving collaterals remained within each hemisphere, forming an early Probst’s bundle-like shape. The early anterior commissure in the brain of jsap1+/+ at E14.5-E15.5 crossed the midline, whereas the anterior commissure in jsap1-/-developed, but was deviated from their normal path before approaching the midline. The axon tracts of the corpus callosum and anterior commissure in the brain of jsap1-/- at E16.5-E17.5 expressed phosphorylated forms of FAK and JNK, however, their expression levels in the axonal tracts were reduced compared to the respective controls in jsap1+/+. Considering the known scaffolding function of JSAP1 for the FAK and JNK pathways, these results suggest that JSAP1 is required for the pathfinding of the developing telencephalic commissures in the early brains.
The Adenylyl Cyclase Encoded by rutabaga Is Required for Larval Molting in Drosophila
손원석,한평림,정연두 한국유전학회 2008 Genes & Genomics Vol.30 No.2
Hormonal control of insect growth and metamorphosis by neuroendocrine system is well established, yet the cellular mechanism underlying the synthesis and release of insect hormones is not clearly understood. Here we report that a novel enhancer detection line, rutlethal-1096, failed to molt from second to third instar larvae, thus showing a lethal phenotype. Molecular cloning indicated that the enhancer detector was inserted in the proximal promoter region of the rut-encoded adenylyl cyclase (AC) gene. Similarly, the known rut alleles, rut1 and rut1084, were also found to be affected mildly in their larval and pupal development. The enriched expression of the reporter gene lacZ was detected in the ring gland that is an insect larval glandular organ secreting various hormones involved in ecdysis. Taken together, our data suggest the rut-encoded AC plays a vital role in larval molting, probably by regulating the function of ring glands. Hormonal control of insect growth and metamorphosis by neuroendocrine system is well established, yet the cellular mechanism underlying the synthesis and release of insect hormones is not clearly understood. Here we report that a novel enhancer detection line, rutlethal-1096, failed to molt from second to third instar larvae, thus showing a lethal phenotype. Molecular cloning indicated that the enhancer detector was inserted in the proximal promoter region of the rut-encoded adenylyl cyclase (AC) gene. Similarly, the known rut alleles, rut1 and rut1084, were also found to be affected mildly in their larval and pupal development. The enriched expression of the reporter gene lacZ was detected in the ring gland that is an insect larval glandular organ secreting various hormones involved in ecdysis. Taken together, our data suggest the rut-encoded AC plays a vital role in larval molting, probably by regulating the function of ring glands.