GPR155: Gene organization, multiple mRNA splice variants and expression in mouse central nervous system

Trifonov, Stefan; Houtani, Takeshi; Shimizu, Jun Ichi; Hamada, Satoko; Kase, Masahiko; Maruyama, Masato; Sugimoto, Tetsuo

doi:10.1016/j.bbrc.2010.05.162

Cited by 19 publications

(27 citation statements)

References 18 publications

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“…An aliquot (1 μL) of the reverse transcription product was PCR‐amplified as previously described (Houtani et al. , 2005; Trifonov et al. , 2009, 2010), with the forward and reverse primers listed in Table 1.…”

Section: Methodsmentioning

confidence: 99%

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Lateral regions of the rodent striatum reveal elevated glutamate decarboxylase 1 mRNA expression in medium‐sized projection neurons

Trifonov

Houtani

Kase

et al. 2012

Eur J of Neuroscience

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The GABA-synthesizing enzymes glutamate decarboxylase (GAD)1 and GAD2 are universally contained in GABAergic neurons in the central nervous system of the mouse and rat. The two isoforms are almost identically expressed throughout the brain and spinal cord. By using in situ hybridization, we found that the mouse lateral striatum concentrates medium-sized projection neurons with high-level expression of GAD1, but not of GAD2, mRNA. This was confirmed with several types of riboprobe, including those directed to the 5'-noncoding, 3'-noncoding and coding regions. Immunohistochemical localization of GAD1 also revealed predominant localization of the enzyme in the same striatal region. The lateral region of the mouse striatum, harboring such neurons, is ovoid in shape and extends between interaural +4.8 and +2.8, and at lateral 2.8 and dorsoventral 2.0. This intriguing region corresponds to the area that receives afferent inputs from the primary motor and sensory cortex that are presumably related to mouth and forelimb representations. The lateral striatum is included in the basal ganglia-thalamocortical loop, and is most vulnerable to various noxious stimuli in the neurodegeneration processes involving the basal ganglia. We have confirmed elevated expression of GAD1 mRNA, but not of GAD2 mRNA, also in the rat lateral striatum. Image analysis favored the view that the regional increase is caused by elevated cellular expression, and that the greatest number of medium-sized spiny neurons were positive for GAD1 mRNA. The GAD1 mRNA distribution in the mouse lateral striatum partially resembled those of GPR155 and cannabinoid receptor type 1 mRNAs, suggesting functional cooperation in some neurons.

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Section: Methodsmentioning

confidence: 99%

“…We have previously shown the preferential expression of GPR155 in the projection neurons, concentrated in the lateral striatum (Trifonov et al. , 2010).…”

Section: Introductionmentioning

confidence: 99%

Lateral regions of the rodent striatum reveal elevated glutamate decarboxylase 1 mRNA expression in medium‐sized projection neurons

Trifonov

Houtani

Kase

et al. 2012

Eur J of Neuroscience

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“…The position of the amino acid substitution found in this study (Asn518Ser, Table 3) does not overlap with the kinase catalytic domain (17–260aa), leucine-zipper motif (280–328aa), or sterile-alpha motif domain (336–410aa). The Gpr155 mRNA is widely expressed in adult mouse tissues and during development, but the function of the Gpr155 protein has not been elucidated [17]. The metaxin 2 protein, a mitochondrial outer membrane protein, is expressed in the mouse liver, kidney, lung, and heart.…”

Section: Discussionmentioning

confidence: 99%

Searching for Genomic Region of High-Fat Diet-Induced Type 2 Diabetes in Mouse Chromosome 2 by Analysis of Congenic Strains

Kobayashi¹,

Ohno²,

Ihara³

et al. 2014

PLoS ONE

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SMXA-5 mice are a high-fat diet-induced type 2 diabetes animal model established from non-diabetic SM/J and A/J mice. By using F2 intercross mice between SMXA-5 and SM/J mice under feeding with a high-fat diet, we previously mapped a major diabetogenic QTL (T2dm2sa) on chromosome 2. We then produced the congenic strain (SM.A-T2dm2sa (R0), 20.8–163.0 Mb) and demonstrated that the A/J allele of T2dm2sa impaired glucose tolerance and increased body weight and body mass index in the congenic strain compared to SM/J mice. We also showed that the combination of T2dm2sa and other diabetogenic loci was needed to develop the high-fat diet-induced type 2 diabetes. In this study, to narrow the potential genomic region containing the gene(s) responsible for T2dm2sa, we constructed R1 and R2 congenic strains. Both R1 (69.6–163.0 Mb) and R2 (20.8–128.2 Mb) congenic mice exhibited increases in body weight and abdominal fat weight and impaired glucose tolerance compared to SM/J mice. The R1 and R2 congenic analyses strongly suggested that the responsible genes existed in the overlapping genomic interval (69.6–128.2 Mb) between R1 and R2. In addition, studies using the newly established R1A congenic strain showed that the narrowed genomic region (69.6–75.4 Mb) affected not only obesity but also glucose tolerance. To search for candidate genes within the R1A genomic region, we performed exome sequencing analysis between SM/J and A/J mice and extracted 4 genes (Itga6, Zak, Gpr155, and Mtx2) with non-synonymous coding SNPs. These four genes might be candidate genes for type 2 diabetes caused by gene-gene interactions. This study indicated that one of the genes responsible for high-fat diet-induced diabetes exists in the 5.8 Mb genomic interval on mouse chromosome 2.

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“…In relation to the aforementioned brain glucocorticoid signaling, we have observed that splice variants of the GR partner steroid receptor coactivator-1 (SRC-1) are major determinants in the effectiveness of GR, with one variant potentiating repression, and the other variants potentiating stimulation of the target gene corticotropin releasing hormone (CRH) in different brain regions (van der Laan et al, 2008; Lachize et al, 2009). Splice variant diversity has been observed for CRH receptor genes (Markovic et al, 2008; Zmijewski and Slominski, 2009), Cannabinoid receptor genes (Ryberg et al, 2005; Liu et al, 2009), and many others (Fagnani et al, 2007; Trifonov et al, 2010). Below we elaborate on yet one more of these examples, that of dopamine receptor D2 splice variants.…”

Section: Aons As Experimental Toolsmentioning

confidence: 99%

Antisense-Mediated RNA Targeting: Versatile and Expedient Genetic Manipulation in the Brain

Zalachoras¹,

Evers²,

Roon‐Mom³

et al. 2011

Front. Mol. Neurosci.

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A limiting factor in brain research still is the difficulty to evaluate in vivo the role of the increasing number of proteins implicated in neuronal processes. We discuss here the potential of antisense-mediated RNA targeting approaches. We mainly focus on those that manipulate splicing (exon skipping and exon inclusion), but will also briefly discuss mRNA targeting. Classic knockdown of expression by mRNA targeting is only one possible application of antisense oligonucleotides (AON) in the control of gene function. Exon skipping and inclusion are based on the interference of AONs with splicing of pre-mRNAs. These are powerful, specific and particularly versatile techniques, which can be used to circumvent pathogenic mutations, shift splice variant expression, knock down proteins, or to create molecular models using in-frame deletions. Pre-mRNA targeting is currently used both as a research tool, e.g., in models for motor neuron disease, and in clinical trials for Duchenne muscular dystrophy and amyotrophic lateral sclerosis. AONs are particularly promising in relation to brain research, as the modified AONs are taken up extremely fast in neurons and glial cells with a long residence, and without the need for viral vectors or other delivery tools, once inside the blood brain barrier. In this review we cover (1). The principles of antisense-mediated techniques, chemistry, and efficacy. (2) The pros and cons of AON approaches in the brain compared to other techniques of interfering with gene function, such as transgenesis and short hairpin RNAs, in terms of specificity of the manipulation, spatial, and temporal control over gene expression, toxicity, and delivery issues. (3) The potential applications for Neuroscience. We conclude that there is good evidence from animal studies that the central nervous system can be successfully targeted, but the potential of the diverse AON-based approaches appears to be under-recognized.

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GPR155: Gene organization, multiple mRNA splice variants and expression in mouse central nervous system

Cited by 19 publications

References 18 publications

Lateral regions of the rodent striatum reveal elevated glutamate decarboxylase 1 mRNA expression in medium‐sized projection neurons

Lateral regions of the rodent striatum reveal elevated glutamate decarboxylase 1 mRNA expression in medium‐sized projection neurons

Searching for Genomic Region of High-Fat Diet-Induced Type 2 Diabetes in Mouse Chromosome 2 by Analysis of Congenic Strains

Antisense-Mediated RNA Targeting: Versatile and Expedient Genetic Manipulation in the Brain

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