Origin and early development of Schwann cells

Abstract

Cellular events leading to the generation of Schwann cells from the neural crest have recently been clarified and it is now possible to outline a relatively simple model of the Schwann cell lineage in the rat and mouse. Neural crest cells have to undergo three main developmental transitions to become mature Schwann cells. These are the formation of Schwann cell precursors from crest cells, the formation of immature Schwann cells from precursors and, lastly, the postnatal and reversible generation of non‐myelin‐ and myelin‐forming Schwann cells. Axonal signals involving neuregulins are important regulators of these events, in particular of the survival, proliferation, and differentiation of Schwann cell precursors. Transcription factors likely to be involved in the developmental transitions are beginning to be identified. These include Oct‐6, Krox‐20, and Pax‐3 but also members of the basic helix‐loop‐helix family, Sox 10, and the cAMP response element binding protein CREB. Microsc. Res. Tech. 41:393–402, 1998. © 1998 Wiley‐Liss, Inc.

Aberrant motor axon projection, acetylcholine receptor clustering, and neurotransmission in cyclin-dependent kinase 5 null mice

“…NRG signaling is a key regulator of Schwann cell survival during the early stages of development via the PI3K͞Akt pathway (28,29). Given our observation that Cdk5 affects NRG͞ErbB signaling (5), we were interested to examine whether the integrity of Schwann cells, an integral component of the NMJ, was affected in Cdk5 Ϫ/Ϫ embryos.…”

“…4H), suggesting that the lack of S100 staining in Cdk5 Ϫ/Ϫ phrenic nerves was likely due to the loss of Schwann cells. Interestingly, the morphology and functions of these Schwann cells and their expression profiles of ErbB receptors are quite different from terminal Schwann cells (18,28,31). It is possible that the absence of defects in terminal Schwann cells of Cdk5 Ϫ/Ϫ embryos is, in part, because of their differential requirement of NRG͞ErbB signaling.…”

C/EBP-δ Induction by gp130 Signaling

“…The response to IL6RIL6 of this cell population has been analyzed at the RNA level by RT-PCR and on gene arrays after 24 and 48 h of treatment. 3 We used viral particles containing the vector for C/EBP-␦-specific siRNAs to knockdown C/EBP-␦ mRNA. We used cells shortly after infection and found that knocking down C/EBP-␦ inhibited P0 mRNA expression.…”

“…Treatment of such cells with IL6RIL6 increases P0 and C/EBP-␦ mRNA levels, as verified by RT-PCR and analysis on DNA-arrays. 3 In this system, the basal level of P0, and C/EBP-␦ mRNAs in the absence of IL6RIL6 is not negligible. To evaluate the role of C/EBP-␦ in P0 mRNA regulation in this system containing precursor glial cells, we infected the cells with viral particles containing pRS-C/EBP-␦2, and control pRS.…”

“…2 Induction of C/EBP-␦ was also observed in dissociated DRGs cells. 3 C/EBP-␦ belongs to a family of transcriptional regulators dimerizing through long leucine zipper domains (14) and known to couple growth factor signal transduction to cellular differentiation in adipocytes (15,16), mammary cells (17,18), and neural cells (19,20). Proteins of the C/EBP family (C/ EBP-␣, -␤, -␥, -␦, -⑀, and -) have a basic DNA binding domain, share 90% homology in the C-terminal end (leucine zipper) and diverge in the N-terminal region (see Refs.…”