Spinal motor axons and neural crest cells use different molecular guides for segmental migration through the rostral half-somite

Abstract

The peripheral nervous system in vertebrates is composed of repeating metameric units of spinal nerves. During development, factors differentially expressed in a rostrocaudal pattern in the somites confine the movement of spinal motor axons and neural crest cells to the rostral half of the somitic sclerotome. The expression patterns of transmembrane ephrin-B ligands and interacting EphB receptors suggest that these proteins are likely candidates for coordinating the segmentation of spinal motor axons and neural crest cells. In vitro, ephrin-B1 has indeed been shown to repel axons extending from the rodent neural tube (Wang & Anderson, 1997). In avians, blocking interactions between EphB3 expressed by neural crest cells and ephrin-B1 localized to the caudal half of the somite in vivo resulted in loss of the rostrocaudal patterning of trunk neural crest migration (Krull et al., 1997). The role of ephrin-B1 in patterning spinal motor axon outgrowth in avian embryos was investigated. Ephrin-B1 protein was found to be expressed in the caudal half-sclerotome and in the dermomyotome at the appropriate time to interact with the EphB2 receptor expressed on spinal motor axons. Treatment of avian embryo explants with soluble ephrin-B1, however, did not perturb the segmental outgrowth of spinal motor axons through the rostral half-somite. In contrast, under the same treatment conditions with soluble ephrin-B1, neural crest cells migrated aberrantly through both rostral and caudal somite halves. These results indicate that the interaction between ephrin-B1 and EphB2 is not required for patterning spinal motor axon segmentation. Even though spinal motor axons traverse the same somitic pathway as neural crest cells, different molecular guidance mechanisms appear to influence their movement.

Implanted Adult Human Dental Pulp Stem Cells Induce Endogenous Axon Guidance

“…Dose‐dependent analyses showed that optimal T140 inhibition of DPSC‐mediated TG axon guidance occurred at 5 μM (data not shown). The human‐chick chimeric embryos 2 hpi were explanted onto Millipore membranes and grown ex ovo in serum‐free defined media [30] supplemented with T140 or control peptide (Figs. 1E, 1F, Fig.…”

“…GFP‐transduced adult human DPSCs (5 × 10 3 cells/μl) were maintained in growth media alone or in the presence of CXCL12/SDF‐1, inhibitor T140 [27–29], or control peptide (RTVAHHGGLYHTNAEVK) (5 μM) (Mimotope, Victoria, Australia) before transplantation into the avian embryo. DPSCs were injected as described above, embryos were then dissected from the egg 2 hours postinjection, washed in Ringer's solution, and explanted onto a Millipore membrane (Millipore, Billerica, MA, http://www.millipore.com), as described previously [30]. The embryos were orientated so that the vitelline membrane (ventral side down) was in contact with the Millipore membrane bathed in Neurobasal Medium (GIBCO BRL, Grand Island, NY, http://www.invitrogen.com), B27 supplement (GIBCO BRL), and 0.5 mM L ‐glutamine (GIBCO BRL) with T140 or control peptide.…”

Nedd1 expression as a marker of dynamic centrosomal localization during mouse embryonic development

“…3). The cells of the DRG arise from the neural crest cells that migrate from the neural tube and undergo a distinct developmental programme (Koblar et al 2000). In neural migration, the centrosome is initially located ahead of the nucleus in the direction of migration (Gregory et al 1988).…”

Draxin, an axon guidance protein, affects chick trunk neural crest migration

“…Eph‐family receptors and their ligands are also involved in interactions between neural crest and sclerotomal cells (Krull et al. 1997; Wang & Anderson 1997; Koblar et al. 2000; McLennan & Krull 2002; Santiago & Erickson 2002; Kasemeier‐Kulesa et al.…”