High-resolution Genetic and Physical Map of theLgn1Interval in C57BL/6J ImplicatesNaip2orNaip5inLegionella pneumophilaPathogenesis

Growney, Joseph D.; Dietrich, William F.

doi:10.1101/gr.10.8.1158

Cited by 59 publications

(43 citation statements)

References 45 publications

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“…The physiological function of the NLR protein NAIP (NLR family apoptosis inhibitory protein, previously known as neuronal apoptosis inhibitory protein) is not fully characterized, mainly because mice have several possibly redundant Naip paralogs (e.g., 4 functional and 2 noncoding Naip genes in the C57BL/6 genome; Yaraghi et al, 1998;Endrizzi et al, 2000;Growney and Dietrich, 2000). Humans also have several NAIP genes, only one of which is full length (Schmutz et al, 2004;Romanish et al, 2009).…”

mentioning

confidence: 99%

Epithelial NAIPs protect against colonic tumorigenesis

Allam¹,

Maillard²,

Tardivel³

et al. 2015

J Cell Biol

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confidence: 99%

Epithelial NAIPs protect against colonic tumorigenesis

Allam¹,

Maillard²,

Tardivel³

et al. 2015

J Cell Biol

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“…The mouse strain-specific variation in permissiveness to Legionella replication is controlled by Lgn1, an autosomal recessive locus on chromosome 13 (9 -11). Genetic studies in mice identified the Naip5/Birc1e gene as the Legionella susceptibility factor (12)(13)(14). There are 14 amino acid substitutions between the C57BL/6 (B6) and A/J Naip5 proteins (15).…”

mentioning

confidence: 99%

The Nod-Like Receptor Family Member Naip5/Birc1e Restricts Legionella pneumophila Growth Independently of Caspase-1 Activation

Lamkanfi

Amer

Kanneganti

et al. 2007

The Journal of Immunology

108

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Similar to Ipaf and caspase-1, the Nod-like receptor protein Naip5 restricts intracellular proliferation of Legionella pneumophila, the causative agent of a severe form of pneumonia known as Legionnaires’ disease. Thus, Naip5 has been suggested to regulate Legionella replication inside macrophages through the activation of caspase-1. In this study, we show that cytosolic delivery of recombinant flagellin activated caspase-1 in A/J macrophages carrying a mutant Naip5 allele, and in C57BL/6 (B6) macrophages congenic for the mutant Naip5 allele (B6-Naip5A/J), but not in Ipaf−/− cells. In line with these results, A/J and B6-Naip5A/J macrophages induced high levels of caspase-1 activation and IL-1β secretion when infected with Legionella. In addition, transgenic expression of a functional Naip5 allele in A/J macrophages did not alter Legionella-induced caspase-1 activation and IL-1β secretion. Notably, defective Naip5 signaling renders B6-Naip5A/J macrophages permissive for Legionella proliferation despite normal caspase-1 activation. These results indicate that the restriction of intracellular Legionella replication is more complex than previously appreciated and requires both Ipaf-dependent caspase-1 activation as well as functional Naip5 signaling.

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“…In addition, the high density of SINEs upstream of IAP genes may be related to the known role of the highly repetitive SINE sequences in facilitating genomic rearrangements [41]. The BIR domain was amplified to create the IAP family, NAIP genes have amplified variably in rodents [19], and two other IAPs, cIAP1 and 2, are tandemly duplicated copies present in primates and rodents [42], implicating ongoing genomic rearrangements in IAP gene expansion. Moreover, while the IAP genes are classified as a gene family due to the shared BIR domain, mouse gene knockout evidence suggests these proteins do not encode entirely overlapping functions.…”

Section: Discussionmentioning

confidence: 99%

“…We conducted 59 RACE on primary B6 colon and liver RNA using primers specific for each NAIP copy (mNaipa/b/c/e/f) [19]. No evidence of mNaipc transcription was detected and it may represent a pseudogene detected through genomic Southern blots [19].…”

Section: Author Summarymentioning

confidence: 99%

Repeated Recruitment of LTR Retrotransposons as Promoters by the Anti-apoptotic Locus NAIP During Mammalian Evolution

Romanish¹,

Lock²,

Lagemaat³

et al. 2005

PLoS Genet

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Neuronal apoptosis inhibitory protein (NAIP, also known as BIRC1) is a member of the conserved inhibitor of apoptosis protein (IAP) family. Lineage-specific rearrangements and expansions of this locus have yielded different copy numbers among primates and rodents, with human retaining a single functional copy and mouse possessing several copies, depending on the strain. Roles for this gene in disease have been documented, but little is known about transcriptional regulation of NAIP. We show here that NAIP has multiple promoters sharing no similarity between human and rodents. Moreover, we demonstrate that multiple, domesticated long terminal repeats (LTRs) of endogenous retroviral elements provide NAIP promoter function in human, mouse, and rat. In human, an LTR serves as a tissue-specific promoter, active primarily in testis. However, in rodents, our evidence indicates that an ancestral LTR common to all rodent genes is the major, constitutive promoter for these genes, and that a second LTR found in two of the mouse genes is a minor promoter. Thus, independently acquired LTRs have assumed regulatory roles for orthologous genes, a remarkable evolutionary scenario. We also demonstrate that 59 flanking regions of IAP family genes as a group, in both human and mouse are enriched for LTR insertions compared to average genes. We propose several potential explanations for these findings, including a hypothesis that recruitment of LTRs near NAIP or other IAP genes may represent a host-cell adaptation to modulate apoptotic responses.

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High-resolution Genetic and Physical Map of theLgn1Interval in C57BL/6J ImplicatesNaip2orNaip5inLegionella pneumophilaPathogenesis

Cited by 59 publications

References 45 publications

Epithelial NAIPs protect against colonic tumorigenesis

Epithelial NAIPs protect against colonic tumorigenesis

The Nod-Like Receptor Family Member Naip5/Birc1e Restricts Legionella pneumophila Growth Independently of Caspase-1 Activation

Repeated Recruitment of LTR Retrotransposons as Promoters by the Anti-apoptotic Locus NAIP During Mammalian Evolution

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