Disease relevance of Sema3f_predicted

• Induction of neuropilins-1 and -2 and their ligands, Sema3A, Sema3F, and VEGF, during Wallerian degeneration in the peripheral nervous system [1].

High impact information on Sema3f_predicted

• In contrast to dendrites, axons were protected from Sema3F-induced collapse when cAMP signaling was inhibited [2].
• Axonal and dendritic growth cones both expressed type 1 adenylyl cyclase, but only axons showed a cAMP increase in response to Sema3F, and the elevated cAMP was sufficient to collapse axonal growth cones [2].
• Activation of cAMP signaling antagonized dendritic collapse induced by the potent repellents Sema3F and glutamate [2].
• At embryonic days 13-15, among members of class 3 semaphorins, only semaphorin 3F (Sema3F) was expressed in the diencephalon [3].
• These results suggest that the growth of axons from the habenular nucleus along the neuromere boundary region may be regulated by Sema3F from the rostral p1, and netrin-1 from the ventral region of the caudal diencephalon [3].

Biological context of Sema3f_predicted

• We now report that in cultured rat Schwann cells, expression of mRNA encoding neuropilin-2 (NRP2) and plexin-A3 (PlexA3), proteins involved in semaphorin-3F (Sema3F) signal transduction, is diminished markedly by forskolin, an adenylate cyclase activator that, like axonal contact, induces Schwann cell synthesis of myelin lipids and proteins [4].
• This latency may result from chemorepulsion by epithelial Sema3A (Dillon et al. (2004) Journal of Comparative Neurology 470, 13-24), or Sema3F, which we report is also expressed in this epithelium [5].

Anatomical context of Sema3f_predicted

• Evidence that Sema3A and Sema3F regulate the migration of GABAergic neurons in the developing neocortex [6].
• We confirmed a prior report (Exp. Neurol. 172 (2001) 398) that VEGF mRNA levels rise during Wallerian degeneration in the PNS and herein demonstrate that NP-1, NP-2, Sema3A, and Sema3F mRNA levels increase in peripheral nerves distal to a transection or crush injury [1].
• In a sciatic nerve crush model, in which axonal regeneration is robust, the highest levels of Sema3F mRNA below the injury site are in the epi- and perineurium [1].
• Distinct roles for Sema3A, Sema3F, and an unidentified trophic factor in controlling the advance of geniculate axons to gustatory lingual epithelium [5].
• NT-4-stimulated neurite outgrowth is sensitive to Sema3A and Sema3F through E18, but NT-4 has not been detected in E15-18 tongue [5].

Other interactions of Sema3f_predicted

• Sema3A and Sema3F repelled or suppressed geniculate neurite outgrowth, respectively, and these effects were stage and neurotrophic factor dependent [5].
• BDNF-stimulated outgrowth is repelled by Sema3A until E17, but insensitive to Sema3F from E16 [5].

References