EMPReSS: standardized phenotype screens for functional annotation of the mouse genome

Brown, Steven W.; Chambon, Pierre; Mh, de Angelis

doi:10.1038/ng1105-1155

Cited by 144 publications

(51 citation statements)

References 10 publications

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“…In contrast, oral administration of LPS is less common, perhaps because it is non-toxic to healthy mice even at doses 16.5X greater than that used here (Harper et al, 2011). Consistent with this report, we did not observe obvious signs of sickness, including changes in body position (hunched back, lying on side, or prone), sustained eye closure, piloerection, dragging or elevated tail position, or failure to respond to finger stroke of the back (Brown et al, 2005, Hines et al, 2013). We recorded these observations, rectal temperature, and body weight between 9:00–10:00 am on day −1 to day 7 post-ingestion in a subset of mice (n=12).…”

Section: Methodssupporting

confidence: 91%

Ingestion of bacterial lipopolysaccharide inhibits peripheral taste responses to sucrose in mice

Zhu

McCluskey

2014

Neuroscience

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A fundamental role of the taste system is to discriminate between nutritive and toxic foods. However, it is unknown whether bacterial pathogens that might contaminate food and water modulate the transmission of taste input to the brain. We hypothesized that exogenous, bacterially-derived lipopolysaccharide (LPS), modulates neural responses to taste stimuli. Neurophysiological responses from the chorda tympani nerve, which innervates taste cells on the anterior tongue, were unchanged by acute exposure to LPS. Instead, neural responses to sucrose were selectively inhibited in mice that drank LPS during a single overnight period. Decreased sucrose sensitivity appeared 7 days after LPS ingestion, in parallel with decreased lingual expression of Tas1r2 and Tas1r3 transcripts, which are translated to T1R2+T1R3 subunits forming the sweet taste receptor. Tas1r2 and Tas1r3 mRNA expression levels and neural responses to sucrose were restored by 14 days after LPS consumption. Ingestion of LPS, rather than contact with taste receptor cells, appears to be necessary to suppress sucrose responses. Furthermore, mice lacking the Toll-like receptor (TLR) 4 for LPS were resistant to neurophysiological changes following LPS consumption. These findings demonstrate that ingestion of LPS during a single period specifically and transiently inhibits neural responses to sucrose. We suggest that LPS drinking initiates TLR4-dependent hormonal signals that downregulate sweet taste receptor genes in taste buds. Delayed inhibition of sweet taste signaling may influence food selection and the complex interplay between gastrointestinal bacteria and obesity.

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Section: Methodssupporting

confidence: 91%

Ingestion of bacterial lipopolysaccharide inhibits peripheral taste responses to sucrose in mice

Zhu

McCluskey

2014

Neuroscience

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“…In parallel, a number of past and ongoing standardized phenotyping projects have documented traits in inbred strains and mutant lines for phenotypes relevant to human disease, including the Mouse Phenome Project, the European Mouse Disease Clinic (EUMODIC) and the Mouse Genetics Project (MGP; based at the Wellcome Trust Sanger Institute); see also Table 2[81-84]. The results from many screens are made available online, enabling researchers to identify potentially interesting phenotypes for detailed analysis (Figure 2).…”

Section: Mouse Genetics On a Grand Scalementioning

confidence: 99%

The mouse genetics toolkit: revealing function and mechanism

et al. 2011

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“…Mice were assessed for dysmorphology as described (European Mouse Phenotyping Resource of Standardised Screens [EMPReSS]) 36. Anaesthetized mice were assessed by digital radiography at 26 kV for 3 s using a Faxitron MX‐20 digital X‐ray system (Faxitron X‐ray Corporation, Lincolnshire, IL, USA)34 and DXA using a Lunar PIXImus densitometer (GE Healthcare, Chalfont St Giles, UK), as reported 37.…”

Section: Methodsmentioning

confidence: 99%

An N‐Ethyl‐N‐Nitrosourea (ENU) Mutagenized Mouse Model for Autosomal Dominant Nonsyndromic Kyphoscoliosis Due to Vertebral Fusion

et al. 2018

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Kyphosis and scoliosis are common spinal disorders that occur as part of complex syndromes or as nonsyndromic, idiopathic diseases. Familial and twin studies implicate genetic involvement, although the causative genes for idiopathic kyphoscoliosis remain to be identified. To facilitate these studies, we investigated progeny of mice treated with the chemical mutagen N‐ethyl‐N‐nitrosourea (ENU) and assessed them for morphological and radiographic abnormalities. This identified a mouse with kyphoscoliosis due to fused lumbar vertebrae, which was inherited as an autosomal dominant trait; the phenotype was designated as hereditary vertebral fusion (HVF) and the locus as Hvf. Micro–computed tomography (μCT) analysis confirmed the occurrence of nonsyndromic kyphoscoliosis due to fusion of lumbar vertebrae in HVF mice, consistent with a pattern of blocked vertebrae due to failure of segmentation. μCT scans also showed the lumbar vertebral column of HVF mice to have generalized disc narrowing, displacement with compression of the neural spine, and distorted transverse processes. Histology of lumbar vertebrae revealed HVF mice to have irregularly shaped vertebral bodies and displacement of intervertebral discs and ossification centers. Genetic mapping using a panel of single nucleotide polymorphic (SNP) loci arranged in chromosome sets and DNA samples from 23 HVF (eight males and 15 females) mice, localized Hvf to chromosome 4A3 and within a 5‐megabase (Mb) region containing nine protein coding genes, two processed transcripts, three microRNAs, five small nuclear RNAs, three large intergenic noncoding RNAs, and 24 pseudogenes. However, genome sequence analysis in this interval did not identify any abnormalities in the coding exons, or exon‐intron boundaries of any of these genes. Thus, our studies have established a mouse model for a monogenic form of nonsyndromic kyphoscoliosis due to fusion of lumbar vertebrae, and further identification of the underlying genetic defect will help elucidate the molecular mechanisms involved in kyphoscoliosis. © 2018 The Authors. JBMR Plus is published by Wiley Periodicals, Inc. on behalf of the American Society for Bone and Mineral Research

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EMPReSS: standardized phenotype screens for functional annotation of the mouse genome

Abstract: Peer reviewe

Cited by 144 publications

References 10 publications

Ingestion of bacterial lipopolysaccharide inhibits peripheral taste responses to sucrose in mice

Ingestion of bacterial lipopolysaccharide inhibits peripheral taste responses to sucrose in mice

The mouse genetics toolkit: revealing function and mechanism

An N‐Ethyl‐N‐Nitrosourea (ENU) Mutagenized Mouse Model for Autosomal Dominant Nonsyndromic Kyphoscoliosis Due to Vertebral Fusion

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