The first intron of the myelin proteolipid protein gene confers cell type-specific expression by a transcriptional repression mechanism in non-expressing cell types

Wight, P.A.L.; Dobretsova, Anna

doi:10.1016/s0378-1119(97)00435-6

Cited by 34 publications

(55 citation statements)

References 29 publications

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“…Mouse CGNs were isolated, purified in a discontinuous Percoll gradient, and cultured as previously described (Dickendesher et al, 2012). N20.1 cells were a gift from Dr Anthony Campagnoni (University of California Los Angeles) and were cultured as previously described (Wight and Dobretsova, 1997).…”

Section: Cell Culturementioning

confidence: 99%

LDL receptor-related protein-1 is a sialic-acid-independent receptor for myelin-associated glycoprotein that functions in neurite outgrowth inhibition by MAG and CNS myelin

Stiles

Dickendesher

Gaultier

et al. 2013

Journal of Cell Science

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SummaryIn the injured adult mammalian central nervous system (CNS), products are generated that inhibit neuronal sprouting and regeneration. In recent years, most attention has focused on the myelin-associated inhibitory proteins (MAIs) Nogo-A, OMgp, and myelin-associated glycoprotein (MAG). Binding of MAIs to neuronal cell-surface receptors leads to activation of RhoA, growth cone collapse, and neurite outgrowth inhibition. In the present study, we identify low-density lipoprotein (LDL) receptor-related protein-1 (LRP1) as a high-affinity, endocytic receptor for MAG. In contrast with previously identified MAG receptors, binding of MAG to LRP1 occurs independently of terminal sialic acids. In primary neurons, functional inactivation of LRP1 with receptor-associated protein, depletion by RNA interference (RNAi) knock-down, or LRP1 gene deletion is sufficient to significantly reverse MAG and myelin-mediated inhibition of neurite outgrowth. Similar results are observed when LRP1 is antagonized in PC12 and N2a cells. By contrast, inhibiting LRP1 does not attenuate inhibition of neurite outgrowth caused by chondroitin sulfate proteoglycans. Mechanistic studies in N2a cells showed that LRP1 and p75NTR associate in a MAG-dependent manner and that MAG-mediated activation of RhoA may involve both LRP1 and p75NTR. LRP1 derivatives that include the complement-like repeat clusters CII and CIV bind MAG and other MAIs. When CII and CIV were expressed as Fc-fusion proteins, these proteins, purified full-length LRP1 and shed LRP1 all attenuated the inhibition of neurite outgrowth caused by MAG and CNS myelin in primary neurons. Collectively, our studies identify LRP1 as a novel MAG receptor that functions in neurite outgrowth inhibition.

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Section: Cell Culturementioning

confidence: 99%

LDL receptor-related protein-1 is a sialic-acid-independent receptor for myelin-associated glycoprotein that functions in neurite outgrowth inhibition by MAG and CNS myelin

Stiles

Dickendesher

Gaultier

et al. 2013

Journal of Cell Science

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“…The assays of IPC synthase activity also confirmed that BcAUR1a counteracted the inhibition of AbA (Table 1, compared with the wild type). Recently, it has been reported that some introns in eukaryotic genes can regulate gene transcription, acting the role of a transcriptional enhancer or suppressor (Bhattacharyya and Banerjee, 1999;Clement and Wilkinson, 2000;Jeong et al, 2009;Surinya et al, 1998;Wight and Dobretsova, 1997). However, a similar phenomenon in BcAUR1a cells has not been observed in other fungi.…”

Section: Discussionmentioning

confidence: 96%

Characteristics of inositol phosphorylceramide synthase and effects of aureobasidin A on growth and pathogenicity of <i>Botrytis cinerea</i>

Wang

Guo

et al. 2015

J. Gen. Appl. Microbiol.

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IntroductionSphingolipids are known to be important components Inositol phosphorylceramide (IPC) synthase is the key enzyme with highly conserved sequences, which is involved in fungal sphingolipid biosynthesis. The antibiotic aureobasidin A (AbA) induces the death of fungi through inhibiting IPC synthase activity. The mutations of AUR1 gene coding IPC synthase in fungi and protozoa causes a resistance to AbA. However, the mechanism of AbA resistance is still elusive. In this paper, we generated two mutants of Botrytis cinerea with AbA-resistance, BcAUR1a and BcAUR1b, through UV irradiation. BcAUR1a lost an intron and BcAUR1b had three amino acid mutations (L197P, F288S and T323A) in the AUR1 gene. AbA strongly inhibits the activity of IPC synthase in wild-type B. cinerea, which leads to distinct changes in cell morphology, including the delay in conidial germination, excessive branching near the tip of the germ tube and mycelium, and the inhibition of the mycelium growth. Further, AbA prevents the infection of wild-type B. cinerea in tomato fruits via reducing oxalic acid secretion and the activity of cellulase and pectinase. On the contrary, AbA has no effect on the growth and pathogenicity of the two mutants. Although both mutants show a similar AbA resistance, the molecular mechanisms might be different between the two mutants.

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“…Dev Neurosci 1998;20:552-558 553 intron did not influence reporter gene expression compared to a similar but 'intronless' construct in transfected glial cells [16]. However, we have also shown that the 5) half of the PLP intron 1 sequences was capable of augmenting reporter gene expression initiated from the herpes simplex-1 virus (HSV) thymidine kinase (TK) basal promoter in both glial and nonglial cells [17].…”

Section: Effects Of Intron 1 Sequences On Plp Gene Transcriptionmentioning

confidence: 82%

“…Taken together, these transgenic results suggest that the proximal 2.4 kb of 5) PLP genomic DNA probably direct cell-type specificity. However, transfection results [15][16][17] with reporter genes under control of the mouse PLP promoter suggest that this possibility is unlikely. Perhaps the cell-type-specific regulation observed in the transgenic experiments discussed above reflects a difference between the species of PLP DNA tested.…”

Section: Introductionmentioning

confidence: 99%

Myelin Proteolipid Protein Intron 1 Sequences Do Not Appear to Enhance Myelin Proteolipid Protein Gene Transcription

Wight

Dobretsova²

1998

Dev Neurosci

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Sequences from the first intron of the mouse myelin proteolipid protein (PLP) gene were examined for their ability to modulate PLP gene expression. Glial (N20.1) or nonglial (NIH 3T3) cells were transiently transfected with constructs that contained 1.4 kb of PLP promoter sequence driving luciferase reporter gene expression, as well as various portions of PLP intron 1 DNA. Although these same PLP intron 1 fragments enhanced reporter gene expression from a heterologous basal promoter in a previous study, the results reported here demonstrate that they do not augment PLP promoter activity. Thus, the regulation of PLP cell-type-specific expression, conferred by the first intron, appears to be mediated by an enhancer-independent mechanism.

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The first intron of the myelin proteolipid protein gene confers cell type-specific expression by a transcriptional repression mechanism in non-expressing cell types

Cited by 34 publications

References 29 publications

LDL receptor-related protein-1 is a sialic-acid-independent receptor for myelin-associated glycoprotein that functions in neurite outgrowth inhibition by MAG and CNS myelin

LDL receptor-related protein-1 is a sialic-acid-independent receptor for myelin-associated glycoprotein that functions in neurite outgrowth inhibition by MAG and CNS myelin

Characteristics of inositol phosphorylceramide synthase and effects of aureobasidin A on growth and pathogenicity of <i>Botrytis cinerea</i>

Myelin Proteolipid Protein Intron 1 Sequences Do Not Appear to Enhance Myelin Proteolipid Protein Gene Transcription

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