scholarly journals Neural cell adhesion molecule regulates cell contact-mediated changes in choline acetyltransferase activity of embryonic chick sympathetic neurons

1988 ◽  
Vol 106 (2) ◽  
pp. 479-486 ◽  
Author(s):  
A Acheson ◽  
U Rutishauser
Keyword(s):  
Choline Acetyltransferase ◽  
Specific Activity ◽  
Ganglion Cells ◽  
Sympathetic Neurons ◽  
Polysialic Acid ◽  
Cell Contact ◽  
Adult Chicken ◽  
Fab Fragments ◽  
Neural Cell Adhesion ◽  
A Cell

E10 chick sympathetic ganglion cells display a cell contact-dependent rise in choline acetyltransferase (ChAT) specific activity over the first several days in culture. This effect can be mimicked by addition of crude membrane fractions prepared from E10 retina and adult chicken brain, but not by those from E10 brain. The effects of both cell-cell and membrane-cell contact are inhibited by the addition of anti-NCAM Fab fragments. The membranes capable of increasing ChAT and those which are ineffective all contain NCAM, however their relative levels of NCAM polysialic acid differ. Whereas membranes with high polysialic acid NCAM are ineffective, selective enzymatic removal of polysialic acid renders them capable of producing an increase in ChAT. The inhibition of NCAM-mediated adhesion produced by Fab fragments can be compensated for by addition of wheat germ agglutinin, but only with membranes whose NCAM has low levels of polysialic acid. Taken together, these data suggest that NCAM can regulate cell contact-mediated increases in ChAT activity. We propose that NCAM-mediated adhesion promotes contact between cell membranes to allow the transmission of an otherwise NCAM-independent signal. In addition, NCAM's polysialic acid moiety appears to influence the ability of cells to transmit this signal, even in the presence of an alternative adhesion mechanism.

scholarly journals Calcium influx into neurons can solely account for cell contact-dependent neurite outgrowth stimulated by transfected L1.

1992 ◽  
Vol 119 (4) ◽  
pp. 883-892 ◽  
Author(s):  
E J Williams ◽  
P Doherty ◽  
G Turner ◽  
R A Reid ◽  
J J Hemperly ◽  
...  
Keyword(s):  
Neurite Outgrowth ◽  
Pc12 Cells ◽  
Calcium Influx ◽  
Polysialic Acid ◽  
Cell Contact ◽  
3T3 Cells ◽  
Cerebellar Neurons ◽  
Calcium Dependent ◽  
Promote Neurite Outgrowth ◽  
Neural Cell Adhesion

We have used monolayers of control 3T3 cells and 3T3 cells expressing transfected human L1 as a culture substrate for rat PC12 cells and rat cerebellar neurons. PC12 cells and cerebellar neurons extended longer neurites on human L1 expressing cells. Neurons isolated from the cerebellum at postnatal day 9 responded equally as well as those isolated at postnatal day 1-4, and this contrasts with the failure of these older neurons to respond to the transfected human neural cell adhesion molecule (NCAM). Human L1-dependent neurite outgrowth could be blocked by antibodies that bound to rat L1 and, additionally, the response could be fully inhibited by pertussis toxin and substantially inhibited by antagonists of L- and N-type calcium channels. Calcium influx into neurons induced by K+ depolarization fully mimics the L1 response. Furthermore, we show that L1- and K+(-)dependent neurite outgrowth can be specifically inhibited by a reduction in extracellular calcium to 0.25 microM, and by pretreatment of cerebellar neurons with the intracellular calcium chelator BAPTA/AM. In contrast, the response was not inhibited by heparin or by removal of polysialic acid from neuronal NCAM both of which substantially inhibit NCAM-dependent neurite outgrowth. These data demonstrate that whereas NCAM and L1 promote neurite outgrowth via activation of a common CAM-specific second messenger pathway in neurons, neuronal responsiveness to NCAM and L1 is not coordinately regulated via posttranslational processing of NCAM. The fact that NCAM- and L1-dependent neurite outgrowth, but not adhesion, are calcium dependent provides further evidence that adhesion per se does not directly contribute to neurite outgrowth.

A Possible Modulation Mechanism of Intramolecular and Intermolecular Interactions for NCAM Polysialylation and Cell Migration

2019 ◽  
Vol 19 (25) ◽  
pp. 2271-2282 ◽  
Author(s):  
Bo Lu ◽  
Xue-Hui Liu ◽  
Si-Ming Liao ◽  
Zhi-Long Lu ◽  
Dong Chen ◽  
...  
Keyword(s):  
Cell Migration ◽  
Intermolecular Interactions ◽  
Mammalian Cells ◽  
Molecular Mechanisms ◽  
Intramolecular Interaction ◽  
Polysialic Acid ◽  
Tumor Cell Migration ◽  
Neural Cell Adhesion ◽  
Polybasic Domains ◽  
Novel Model

Polysialic acid (polySia) is a novel glycan that posttranslationally modifies neural cell adhesion molecules (NCAMs) in mammalian cells. Up-regulation of polySia-NCAM expression or NCAM polysialylation is associated with tumor cell migration and progression in many metastatic cancers and neurocognition. It has been known that two highly homologous mammalian polysialyltransferases (polySTs), ST8Sia II (STX) and ST8Sia IV (PST), can catalyze polysialylation of NCAM, and two polybasic domains, polybasic region (PBR) and polysialyltransferase domain (PSTD) in polySTs play key roles in affecting polyST activity or NCAM polysialylation. However, the molecular mechanisms of NCAM polysialylation and cell migration are still not entirely clear. In this minireview, the recent research results about the intermolecular interactions between the PBR and NCAM, the PSTD and cytidine monophosphate-sialic acid (CMP-Sia), the PSTD and polySia, and as well as the intramolecular interaction between the PBR and the PSTD within the polyST, are summarized. Based on these cooperative interactions, we have built a novel model of NCAM polysialylation and cell migration mechanisms, which may be helpful to design and develop new polysialyltransferase inhibitors.

Choline acetyltransferase immunoreactive sympathetic ganglion cells in a teleost, Stephanolepis cirrhifer

2002 ◽  
Vol 99 (1) ◽  
pp. 31-39 ◽  
Author(s):  
Kengo Funakoshi ◽  
Yoshitoshi Atobe ◽  
Tatsuya Hisajima ◽  
Masato Nakano ◽  
Tetsuo Kadota ◽  
...  
Keyword(s):  
Choline Acetyltransferase ◽  
Sympathetic Ganglion ◽  
Ganglion Cells ◽  
Stephanolepis Cirrhifer

Does early enucleation affect the decussation pattern of alpha cells in the ferret?

1994 ◽  
Vol 11 (3) ◽  
pp. 447-454 ◽  
Author(s):  
Benjamin E. Reese ◽  
Janal L. Urich
Keyword(s):  
Cell Death ◽  
Ganglion Cells ◽  
Alpha Cell ◽  
Alpha Cells ◽  
Naturally Occurring ◽  
Cell Class ◽  
Selective Elimination ◽  
A Cell ◽  
Decussation Pattern ◽  
Binocular Competition

AbstractNaturally occurring cell death has been hypothesized to sculpt various features of the organization of the mature visual pathways, including the recent proposal that the selective elimination of ganglion cells in the temporal retina shapes the formation of decussation patterns. Through a class-specific interocular competition, ganglion cells in the two temporal hemiretinae are selectively lost to produce the decussation patterns characteristic of each individual cell class (Leventhal et al., 1988). The present study has tested this hypothesis by asking whether the removal of one retina in newborn ferrets, which should disrupt binocular interactions at the level of the terminals, alters the decussation pattern of the alpha cells, a cell class that is entirely decussating in the normal adult ferret. Enucleation on the day of birth was found to increase the uncrossed projection by ≈50%, but not a single uncrossed alpha cell was found in the temporal retina. Either alpha cells never project ipsilaterally during development, or if they do, they cannot be rescued by early enucleation. While naturally occurring cell death plays many roles during development, creating the decussation pattern of the ferreth's alpha cell class via a binocular competition at the level of the targets is unlikely to be one of them.

scholarly journals Spa33, a Cell Surface-Associated Subunit of the Mxi-Spa Type III Secretory Pathway of Shigella flexneri, Regulates Ipa Protein Traffic

2001 ◽  
Vol 69 (4) ◽  
pp. 2180-2189 ◽  
Author(s):  
Raymond Schuch ◽  
Anthony T. Maurelli
Keyword(s):  
Cell Surface ◽  
Secretory Pathway ◽  
Shigella Flexneri ◽  
Mobile Element ◽  
Cell Contact ◽  
Protein Traffic ◽  
Type Iii ◽  
Transmembrane Channel ◽  
A Cell ◽  
Spa Type

ABSTRACT The Mxi-Spa type III secretion system of Shigella flexneri directs the host cell contact-induced secretion of a set of invasins, referred to as Ipas. In this study, we examined the role of Spa33 in Ipa secretion. A spa33-null mutant was both noninvasive and unable to translocate the Ipas from inner membrane to outer membrane (OM) positions of the Mxi-Spa transmembrane channel. Spa33 was found to be a Mxi-Spa substrate that is translocated to the bacterial cell surface upon the induction of Ipa secretion. This mobility may serve to drive Ipa translocation within Mxi-Spa toward OM positions. Consistent with a second distinct role in regulating Ipa traffic, the overexpression of Spa33 also blocked Ipa secretion and resulted in Ipa accumulation at the OM. Co-overexpression of Spa33 and another OM-associated element, Spa32, did not disrupt Ipa secretion, suggesting an interaction between the two proteins and an effect on the mechanism which serves to regulate Ipa release from the OM. These findings indicate that Spa33 is a mobile element within Mxi-Spa, which is required to control Ipa translocation into and out of OM positions of the secretory structure.

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