The tenascin gene family in axon growth and guidance

Abstract

Glial cells are thought to play an important role in the regulation of neural pattern formation, e.g. by guiding migrating neuroblasts and growth cones to their target regions. In addition to these supportive roles, astro- and oligodendroglia have also been attributed inhibitory functions. Thus, these lineages are believed to constrain the pathways of migrating neurons and growth cones. Recent studies have led to the current view that the inhibitory roles of the glia of the central nervous system (CNS) may be important for neural pattern formation. Furthermore, inhibitory effects of glia may play an essential role in the failure of CNS regeneration, e.g. in the astrocytic scar. Advances have been made in deciphering the molecular basis of glia-mediated inhibitory influences in the CNS. The present review focuses on the tenascin gene family of extracellular matrix glycoproteins. Of these, tenascin-C and -R are expressed in developing and lesioned neural tissue and embody both stimulatory and anti-adhesive or inhibitory properties for axon growth.

Radial migration of developing microglial cells in quail retina: A confocal microscopy study

“…However, microglial cells that ramify at L1 can then resume their radial migration to reach L2 (interface between sublayers within the IPL) and L3 (IPL-INL interface) by traversing the tenascinrich territory of the IPL. This would be explained by the presence in the tenascin molecule of domains with opposite functions, adhesive and antiadhesive Norenberg et al, 1995;Faissner, 1997;Ghert et al, 2001), and by the ability of this molecule to bind to different receptors (Schnapp et al, 1995;Mackie, 1997;Zacharias et al, 1999;Pesheva and Probstmeier, 2000). Therefore, tenascin is able to exert both inhibitory and stimulatory effects on cell migration (Faissner, 1997).…”

“…This would be explained by the presence in the tenascin molecule of domains with opposite functions, adhesive and antiadhesive Norenberg et al, 1995;Faissner, 1997;Ghert et al, 2001), and by the ability of this molecule to bind to different receptors (Schnapp et al, 1995;Mackie, 1997;Zacharias et al, 1999;Pesheva and Probstmeier, 2000). Therefore, tenascin is able to exert both inhibitory and stimulatory effects on cell migration (Faissner, 1997). Nevertheless, further experimental research is needed to test the hypothesis that tenascin is involved in the stopping and ramification of radially migrating microglial cells.…”

CALEB Binds via Its Acidic Stretch to the Fibrinogen-like Domain of Tenascin-C or Tenascin-R and Its Expression Is Dynamically Regulated after Optic Nerve Lesion

“…A fibrinogen-like module is located at the carboxyl terminus (12)(13)(14)(15). To identify domains of TN-C and TN-R responsible for binding to CALEB, we expressed CALEB construct C1 (Fig.…”

“…CALEB is able to interact both with tenascin-C (TN-C) and tenascin-R (TN-R), members of the tenascin family of ECM proteins. These are large glycoproteins composed of a cysteine-rich region at the amino terminus, multiple EGF-like repeats of the tenascin subtype, several fibronectin type III (FNIII)-like repeats, and a single carboxyl-terminal globe similar to the globular parts of the ␥ and ␤ chains of fibrinogen (12)(13)(14)(15). TN-C and TN-R associate to hexamers and trimers, respectively, mediated by heptad repeats within the aminoterminal cysteine-rich segment.…”

Predicting rates of cell state change caused by stochastic fluctuations using a data-driven landscape model

“…TN-C, which is controlled by a large promoter sequence with a number of transcription factor binding sites (Fig. S1), is highly regulated both temporally and spatially during development, and in the adult, it is expressed predominantly under conditions of wound healing and tumor growth (25)(26)(27) and in hypertensive arteries (28), where it supports vascular smooth muscle cell proliferation, migration, and survival (29,30). In our experiments, a clonal population of cells is grown under homogeneous conditions but exhibits a wide range of GFP intensities, most likely because of noise in promoter activity.…”