Plasmolipin: genomic structure, chromosomal localization, protein expression pattern, and putative association with Bardet-Biedl syndrome

Hamacher, Michael; Pippirs, U.; Köhler, Angelika; Müller, Hans; Bosse, Frank

doi:10.1007/s00335-001-3035-5

Cited by 23 publications

(30 citation statements)

References 37 publications

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“…as MAG (FC of 38), MOBP (FC of 24), plasmolipin (PLLP, FC of 23), claudin 11 (CLDN11, FC of 14), PAQR6 (FC of 13), myelin basic protein (MBP, FC of 12), fatty acid 2-hydroxylase (FA2H, FC of 10), and gap junction protein beta 1 (GJP1, FC of 8) (52,(76)(77)(78)(79). Other highly downregulated genes include ABCA2 (FC of 16), which was also significantly downregulated at 3 dpi, and the lipidanchored membrane paralemmin (PALM, FC of 8), which regulates neuron cell shape and motility (80).…”

Section: Fig 7 Immunohistochemistry Gene Validation Ihc Staining Andmentioning

confidence: 99%

Acute Simian Varicella Virus Infection Causes Robust and Sustained Changes in Gene Expression in the Sensory Ganglia

Arnold

Girke

Sureshchandra

et al. 2016

J Virol

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Primary infection with varicella-zoster virus (VZV), a neurotropic alphaherpesvirus, results in varicella. VZV establishes latency in the sensory ganglia and can reactivate later in life to cause herpes zoster. The relationship between VZV and its host during acute infection in the sensory ganglia is not well understood due to limited access to clinical specimens. Intrabronchial inoculation of rhesus macaques with simian varicella virus (SVV) recapitulates the hallmarks of VZV infection in humans. We leveraged this animal model to characterize the host-pathogen interactions in the ganglia during both acute and latent infection by measuring both viral and host transcriptomes on days postinfection (dpi) 3, 7, 10, 14, and 100. SVV DNA and transcripts were detected in sensory ganglia 3 dpi, before the appearance of rash. CD4 and CD8 T cells were also detected in the sensory ganglia 3 dpi. Moreover, lung-resident T cells isolated from the same animals 3 dpi also harbored SVV DNA and transcripts, suggesting that T cells may be responsible for trafficking SVV to the ganglia. Transcriptome sequencing (RNA-Seq) analysis showed that cessation of viral transcription 7 dpi coincides with a robust antiviral innate immune response in the ganglia. Interestingly, a significant number of genes that play a critical role in nervous system development and function remained downregulated into latency. These studies provide novel insights into host-pathogen interactions in the sensory ganglia during acute varicella and demonstrate that SVV infection results in profound and sustained changes in neuronal gene expression. IMPORTANCEMany aspects of VZV infection of sensory ganglia remain poorly understood, due to limited access to human specimens and the fact that VZV is strictly a human virus. Infection of rhesus macaques with simian varicella virus (SVV), a homolog of VZV, provides a robust model of the human disease. Using this model, we show that SVV reaches the ganglia early after infection, most likely by T cells, and that the induction of a robust innate immune response correlates with cessation of virus transcription. We also report significant changes in the expression of genes that play an important role in neuronal function. Importantly, these changes persist long after viral replication ceases. Given the homology between SVV and VZV, and the genetic and physiological similarities between rhesus macaques and humans, our results provide novel insight into the interactions between VZV and its human host and explain some of the neurological consequences of VZV infection. V aricella-zoster virus (VZV) is a neurotropic alphaherpesvirus and the causative agent of varicella (chickenpox) (1). VZV establishes latency in the sensory ganglia and can reactivate later in life to cause herpes zoster (shingles), a painful disease that affects almost 1 million individuals in the United States alone (2). VZV is transmitted through the inhalation of virus-laden saliva droplets or by direct contact with the infectious fluid from vesicles...

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Section: Fig 7 Immunohistochemistry Gene Validation Ihc Staining Andmentioning

confidence: 99%

Acute Simian Varicella Virus Infection Causes Robust and Sustained Changes in Gene Expression in the Sensory Ganglia

Arnold

Girke

Sureshchandra

et al. 2016

J Virol

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“…EGFP, enhanced green fluorescent protein, 29 kDa, isolated from the PMP22-transfected HeLa cells; PLA, plasmolipin, 20 kDa; PMP, peripheral myelin protein 22, 22 kDa;and P0, protein zero, 30 kDa. 1990;Sapirstein et al, 1991) myelin, apical kidney membranes, and other tissues containing polarized cells (Gillen et al, 1996;Hamacher et al, 2001). Furthermore, plasmolipin shares some sequence similarities with MAL (Magyar et al, 1997;Perez et al, 1997).…”

Section: Discussionmentioning

confidence: 94%

“…Polyclonal anti-PMP22 antibody (1:300; D'Urso and Müller, 1997), polyclonal anti-plasmolipin antibody (1:200; Hamacher et al, 2001), polyclonal anti-P0 antibody (1:500; Antibody Service, Dr. Pineda, Berlin, Germany), monoclonal anti-MBP antibody (1:3,000, Chemicon, Hofheim, Germany), monoclonal anti-GFP antibody (1:500, Clontech, Heidelberg, Germany), and monoclonal anti-P0 antibody (1:10,000; Archelos et al, 1993).…”

Section: Antibodiesmentioning

confidence: 99%

Proteins of peripheral myelin are associated with glycosphingolipid/cholesterol‐enriched membranes

Hasse

Bosse

Müller

2002

J of Neuroscience Research

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A characteristic feature of the vertebrate nervous system is the ensheathment of axons by myelin, a multilamellar membrane specialization produced by polarized glial cells. Although the main protein and lipid components of the myelin sheath are well characterized, relatively little is known about the mechanisms of their intracellular distribution to the respective sites of assembly within the myelin sheath. To analyze whether peripheral myelin protein trafficking is mediated by glycosphingolipid/cholesterol-enriched membranes (GEMs), we studied the association of established myelin proteins, peripheral myelin protein 22 (PMP22), protein zero (P0), plasmolipin, and myelin basic protein (MBP), with these membrane microdomains. To examine the association of the selected peripheral myelin proteins with detergent-insoluble GEMs, purified myelin from sciatic nerve of adult rat was extracted with Triton X-100 at 4 degrees C and 37 degrees C and, in additional experiments, was pretreated with the cholesterol chelator methyl-beta-cyclodextrin. The material was then centrifuged to equilibrium in sucrose gradients, and fractions were analyzed by Western blotting. Here we demonstrate for the first time that PMP22, P0, and plasmolipin prepared from purified peripheral myelin are associated with GEMs. To characterize whether the association of these proteins is a specialized feature of myelinating Schwann cells, we studied the distribution of PMP22, P0, and plasmolipin in transiently transfected HeLa cells. These experiments confirm the specific association of these proteins with GEMs in both neural and nonneural cell types.

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“…Hamacher et al (15) previously localized the hPLLP gene to chromosome 16q13 by using PLLP gene-specific PCR and genomic DNA from the same G3 human-hamster RH cell lines that we have used here. Their analysis of DNA from all 83 RH cell lines localized the PLLP gene closest to the marker SHGC-34581, with an LOD score of 11.48.…”

Section: Discussionmentioning

confidence: 99%

“…PLLP is a major component of myelin (4,10), is present in the apical membranes of tubular epithelial cells, and has been detected in a variety of other tissues (3,15). PLLP can be extracted from membranes using organic solvents and, upon its addition to synthetic lipid bilayers, can induce the formation of ion channels that are both voltage dependent and potassium specific (43).…”

Section: Discussionmentioning

confidence: 99%

Identification of the Myelin Protein Plasmolipin as the Cell Entry Receptor forMus caroliEndogenous Retrovirus

Miller

Bergholz

Ziegler

et al. 2008

J Virol

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The Asian wild mouse species Mus caroli harbors an endogenous retrovirus (McERV) that is closely related to but distinct from the endogenous retrovirus family defined by the Mus dunni endogenous virus and the Mus musculus endogenous retrovirus. McERV could infect some cell types from humans, dogs, and rats, but not all, and did not infect any mouse cell line tested. Because of its interesting host range and proposed ancestral relationship to primate retroviruses and because none of the entry receptors for this family of retroviruses had been identified, we began a search for the McERV receptor. We determined the chromosomal location of the receptor gene in the human genome by phenotypic screening of the G3 human-hamster radiation hybrid cell line panel and confirmed the localization by assaying for receptor activity conferred by bacterial artificial chromosome (BAC) clones spanning the region. We next localized the gene more precisely in one positive BAC by assaying for receptor activity following BAC digestion with several restriction enzymes that cleaved different sets of genes, and we confirmed that the final candidate gene, plasmolipin (PLLP; TM4SF11), is the novel receptor by showing that the expression of the human PLLP cDNA renders hamster and mouse cells susceptible to McERV infection. PLLP functions as a voltage-dependent potassium ion channel and is expressed primarily in kidney and brain, helping to explain the limited range of cell types that McERV can infect. Interestingly, mouse PLLP also functioned well as a receptor for McERV but was simply not expressed in the mouse cell types that we originally tested.An endogenous gammaretrovirus can be induced from cells of the Asian wild mouse Mus caroli by treatment of the cells with bromodeoxyuridine (22). This virus is distinct from the murine leukemia virus (MuLV) family of active retroviruses found in the laboratory mouse Mus musculus and appeared to be similar to exogenous retroviruses from gibbon apes (gibbon ape leukemia virus [GALV]) and woolly monkeys (simian sarcoma-associated virus [SSAV]). These similarities included a xenotropic host range (the ability to infect cells from species other than mice but not cells from mice) and reported cross interference between the viruses, indicative of a common cell entry receptor. It was therefore hypothesized that mice were the source of the exogenous simian viruses. Recently, a retrovirus induced by bromodeoxyuridine treatment of Mus caroli (Mus caroli endogenous retrovirus [McERV]) that has properties similar to those of the original virus studied over 30 years ago (22) was cloned and sequenced (C. Stocking, M. Ziegler, U. Bergholz, K. Weber, M. Eiden, and V. Prassolov, unpublished results). However, further analysis indicated that McERV does not use the cell entry receptor used by GALV and SSAV (Pit1; Slc20a1), weakening the argument that McERV is the progenitor of GALV and/or SSAV. McERV also did not use the receptors for xenotropic MuLV (Xpr1) (Mus musculus) or those for the endogenous feline leukemia v...

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Plasmolipin: genomic structure, chromosomal localization, protein expression pattern, and putative association with Bardet-Biedl syndrome

Cited by 23 publications

References 37 publications

Acute Simian Varicella Virus Infection Causes Robust and Sustained Changes in Gene Expression in the Sensory Ganglia

Acute Simian Varicella Virus Infection Causes Robust and Sustained Changes in Gene Expression in the Sensory Ganglia

Proteins of peripheral myelin are associated with glycosphingolipid/cholesterol‐enriched membranes

Identification of the Myelin Protein Plasmolipin as the Cell Entry Receptor forMus caroliEndogenous Retrovirus

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