Intrasynovial adhesions were evident between the tendon and the tendon sheath. At the sites of adhesion formation the tendons were acellular but the sheath displayed mild hyperplasia. These observations are consistent with cells moving out of the injury site where the BM-epithelium is damaged. Laminin was distributed throughout the adhesion and on its surface. Of interest, the presence of an intact BM containing a continuous layer of laminin on the surface of the adhesion would explain the longterm stability of these structures. In conclusion, the results show the importance of the tendon epithelium in maintaining the functional integrity of the tendon. Furthermore, the results suggest that engineered tendons lacking a BM-epithelium or transplanted tendons with damaged surfaces, might have limited use in tissue engineering and in vivo regenerative Nodakenin medicine. In the vertebrate nervous system, the rapid and efficient transmission of electrical impulses along many axons requires the presence of an insulating myelin sheath. In the central nervous system, the myelin sheath is formed by a population of glial cells known as oligodendrocytes. Within the spinal cord, most oligodendrocytes arise from a ventral region known as the pMN domain, which also gives rise to motor neurons and interneurons. Once specified, oligodendrocyte progenitor cells migrate out of the pMN domain toward their target axons in the lateral spinal cord. These OPCs divide and extend multiple fine membrane processes as they migrate. Upon reaching their target axons, OPCs stop dividing and extend processes that contact and wrap multiple axons in tube-like structures that are then compacted to form the myelin sheath. The mechanisms that pattern the dorsoventral axis of the neural tube to Morroniside establish pMN precursors are thoroughly described. By contrast, the mechanisms that specify OPCs from pMN precursors and regulate their subsequent division, migration and differentiation to myelinating cells are poorly understood. In an effort to fill this gap we conducted an ENU based mutagenesis screen in zebrafish carrying the Tg reporter, which labels pMN precursors and oligodendrocyte lineage cells.