Myelin

The developmental regulation of sulfogalactosylceramide (sulfatide) synthesis, 2', 3'-cyclic nucleotide-3'-phosphohydrolase activity (CNP), and myelin basic protein (MBP) accumulation, three markers characteristic of myelinogenesis, were observed in dispersed cultures of fetal rat brain in spite of the absence of the formation of compact, multilamellar myelin. Sulfatide synthetic rate and CNP activity began to increase by 8 days in vitro (DIV) (approximately comparable to days post-natal) and reached their maxima by 20 DIV. MBP began to accumulate after 14 DEV and reached a maximum by 38 DIV. Thus, the temporal regulation of the onset of expression of these parameters, which is coordinate in vivo, has been dissociated into two sequential periods in vitro. Similarly, the regulatory mechanisms controlling the subsequent decline of the net expression of these three parameters were dissociated. Whereas, the increase in the net CNP activity ceased on schedule, the decline of sulfatide synthetic rate was delayed 20 days, and the accumulation of MBP underwent a net loss. These data suggest that there are multiple parallel but separate mechanisms of temporal regulation controlling myelinogenic gene expression, and that, among them, those factors that control MBP accumulation are more sensitive to disruption by the rigors of dissociated culture.

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Interaction of ganglioside G_M1 and myelin basic protein studied by carbon‐13 and proton nuclear magnetic resonance spectroscopy

Ong

1984

J of Neuroscience Research

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The interaction of the myelin basic protein (MBP) and the major endogenous ganglioside GM1 in myelin of the central nervous system has been investigated using both 500-MHz 1H and 67.89 MHz 13C NMR. Titration of MBP by GM1 resulted in 13C NMR signal shifts for the I1e and His residues of MBP at a GM1/MBP mole ratio of one or less. The carbohydrate head group of GM1 was also found to be perturbed. 1H NMR results obtained in a similar manner demonstrated the perturbation of His and Phe residues. At a GM1/MBP mole ratio of 0.5, small perturbation of Trp #116 was observed, and at mole ratios of two and beyond significant involvement of Phe residues and methylated Arg #107 was found. Met #167 was more perturbed than Met #20; hence, more extensive interaction of the lipid is occurring with the C-terminus of the protein than with the N-terminus. No resonances from GM1 bound to MBP at mole ratios of up to one appeared in the spectra. However, as the GM1/MBP mole ratio was increased to eight or greater a major conformational change of MBP was detected. An upfield shift of the GM1 midchain methylene resonance was observed for the GM1/MBP complex. This observation provides strong evidence that the state of GM1 interacting with MBP is different from that of GM1 micelles. The number of saturable GM1 binding sites on MBP is estimated to be four. The data also favor a rapid exchange between bound GM1 and GM1 micelles. Interaction of MBP with the oligosaccharide derived from GM1 was found to be weaker than with GM1. Based on our data, a model for the interaction can be proposed: the first GM1 molecule is bound to the protein molecule through its head group and hydrocarbon chains, followed by the formation of a GM1/MBP complex with a concomitant conformational change of MBP as more GM1 is added.

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Myelin

Abstract: Main entry under title: Myelin. Includes index. 1. Demyelination. 2. Myelin. I. Morell, Pierre, 1941sheath. 2. Myelin sheath-pathology. WL102 M994] RC365.M93 616.8'7 ISBN 978-1-4615-7516-0 ISBN 978-1-4615-7514-6 (eBook)

Cited by 17 publications

References 497 publications

Peripheral neuropathy in the cherry‐red spot—myoclonus syndrome (Sialidosis type I)

Peripheral neuropathy in the cherry‐red spot—myoclonus syndrome (Sialidosis type I)

Noncoordinate regulation of myelinogenic parameters in primary cultures of dissociated fetal rat brain

Interaction of ganglioside G_M1 and myelin basic protein studied by carbon‐13 and proton nuclear magnetic resonance spectroscopy

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Myelin

Abstract: Main entry under title: Myelin. Includes index. 1. Demyelination. 2. Myelin. I. Morell, Pierre, 1941sheath. 2. Myelin sheath-pathology. WL102 M994] RC365.M93 616.8'7 ISBN 978-1-4615-7516-0 ISBN 978-1-4615-7514-6 (eBook)

Cited by 17 publications

References 497 publications

Peripheral neuropathy in the cherry‐red spot—myoclonus syndrome (Sialidosis type I)

Peripheral neuropathy in the cherry‐red spot—myoclonus syndrome (Sialidosis type I)

Noncoordinate regulation of myelinogenic parameters in primary cultures of dissociated fetal rat brain

Interaction of ganglioside GM1 and myelin basic protein studied by carbon‐13 and proton nuclear magnetic resonance spectroscopy

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Interaction of ganglioside G_M1 and myelin basic protein studied by carbon‐13 and proton nuclear magnetic resonance spectroscopy