Tools and strategies for physiological genomics: the Rat Genome Database

Twigger, Simon; Pasko, Dean; Nie, Jeff; Shimoyama, Mary; Bromberg, Susan K.; Campbell, Dan H.; Chen, Jiali; Cruz, Norberto dela; Chen, Fan; Foote, Cindy; Harris, Glenn; Hickmann, Brian; Ji, Yuan; Jin, Weihong; Li, Dawei; Mathis, Jedidiah; Nenasheva, Nataliya; Nigam, Rajni; Petri, Victoria; Reilly, Dorothy; Ruotti, Victor; Schauberger, Eric; Seiler, K. A.; Slyper, Ronit; Smith, Jennifer S.; Wang, Wei‐Ye; Wu, Wenhua; Zhao, Lan; Zuniga-Meyer, Angela; Tonellato, Peter J.; Kwitek, Anne E.; Jacob, Howard J.

doi:10.1152/physiolgenomics.00040.2005

Cited by 24 publications

(17 citation statements)

References 22 publications

(10 reference statements)

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“…Such expression QTLs would be good candidates for QTLs that influence the actual cellular or organismal phenotype. Numerous genetical genomics papers followed the vision of Jansen and Nap using yeast [82][83][84], Drosophila [85] mice, maize, and human families [86], rats [87] and rodent RI (recombinant inbred) strains [88][89][90].…”

Section: Neurophysiological Process: Gabaergic Systemsmentioning

confidence: 99%

Ventral Tegmental Transcriptome Response to Intermittent Nicotine Treatment and Withdrawal in BALB/cJ, C57BL/6ByJ, and Quasi-Congenic RQI Mice

et al. 2007

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The aim of this study was to identify neurochemical pathways and candidate genes involved in adaptation to nicotine treatment and withdrawal. Locomotor sensitization was assessed in a nicotine challenge test after exposure to intermittent nicotine treatment and withdrawal. About 24 h after the challenge test the ventral tegmentum of the mesencephaion was dissected and processed using oligonucleotide microarrays with 22,690 probe sets (Affymetrix 430A 2.0). Quasi-congenic RQI, and donor BALB/cJ mice developed significant locomotor sensitization, while sensitization was not significant in the background partner, C57BL/6By. Comparing saline treated controls of C57BL/6ByJ and BALB/cJ by a rigorous statistical microarray analysis method we identified 238 differentially expressed transcripts. Quasi-congenic strains B6.Cb4i5-alpha4/Vad and B6.Ib5i7-beta25A/Vad significantly differed from the background strain in 11 and 11 transcripts, respectively. Identification of several cis- and trans-regulated genes indicates that further work with quasi-congenic strains can quickly lead to mapping of Quantitative Trait Loci for nicotine susceptibility because donor chromosome regions have been mapped in quasi-congenic strains. Nicotine treatment significantly altered the abundance of 41, 29, 54, and 14 ventral tegmental transcripts in strains C57BL/6ByJ, BALB/cJ, B6.Cb4i5-alpha4/Vad, and B6.Ib5i7-beta25A/Vad, respectively. Although transcript sets overlapped to some extent, each strain showed a distinct profile of nicotine sensitive genes, indicating genetic effects on nicotine-induced gene expression. Nicotine-responsive genes were related to processes including regulation of signal transduction, intracellular protein transport, proteasomal ubiquitin-dependent protein catabolism, and neuropeptide signaling pathway. Our results suggest that while there are common regulatory mechanisms across inbred strains, even relatively small differences in genetic constitution can significantly affect transcriptome response to nicotine.

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Section: Neurophysiological Process: Gabaergic Systemsmentioning

confidence: 99%

Ventral Tegmental Transcriptome Response to Intermittent Nicotine Treatment and Withdrawal in BALB/cJ, C57BL/6ByJ, and Quasi-Congenic RQI Mice

et al. 2007

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“…Two recent papers describe the tools and data available at RGD. The first describes strategies for using RGD in support of specific research areas including comparative genomics, positional cloning and microarray with a particular focus on using the RGD tools to access data useful in these types of studies (13). A chapter is also available in Current Protocols in Bioinformatics which provides a more step-by-step practical guide to using RGD and its various resources (14).…”

Section: Outreachmentioning

confidence: 99%

The Rat Genome Database, update 2007--Easing the path from disease to data and back again

Twigger¹,

Shimoyama²,

Bromberg³

et al. 2007

Nucleic Acids Research

116

114

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The Rat Genome Database (RGD, ) is one of the core resources for rat genomics and recent developments have focused on providing support for disease-based research using the rat model. Recognizing the importance of the rat as a disease model we have employed targeted curation strategies to curate genes, QTL and strain data for neurological and cardiovascular disease areas. This work has centered on rat but also includes data for mouse and human to create ‘disease portals’ that provide a unified view of the genes, QTL and strain models for these diseases across the three species. The disease curation efforts combined with normal curation activities have served to greatly increase the content of the database, particularly for biological information, including gene ontology, disease, pathway and phenotype ontology annotations. In addition to improving the features and database content, community outreach has been expanded to demonstrate how investigators can leverage the resources at RGD to facilitate their research and to elicit suggestions and needs for future developments. We have published a number of papers that provide additional information on the ontology annotations and the tools at RGD for data mining and analysis to better enable researchers to fully utilize the database.

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“…The rat is another excellent potential model for identifying the genetic causes of human or mouse phenotypes, since there is a wealth of physiological data for the rat. The Rat Genome Database (RGD) is the essential resource for rat genes and genomic data (Twigger et al, 2005) and they aim to adopt the approved nomenclature of human and mouse genes for each rat ortholog.…”

Section: Standardised Nomenclaturementioning

confidence: 99%