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Mitochondrial DNA, Early Online: 1–2! 2014 Informa UK Ltd. DOI: 10.3109/19401736.2014.958692

MITOGENOME ANNOUNCEMENT

Complete mitochondrial genome sequence of the Rattus norvegicusSILN strain with central nervous system disorder

Yu-Zhen Zhang1,2, Ji-Yu Lou2, Chang-Meng Zhang3, Jin-Feng Li1, Hong-Lei Yin1, and Yun-Liang Wang1

1Department of Neurology, The 148th Hospital of PLA, Zibo, P.R. China, 2Department of Neurology, The Second Affiliated Hospital of Zhengzhou

University, Zhengzhou, P.R. China, and 3Department of Orthopedics, The Central Hospital of Zhengzhou City, Zhengzhou, P.R. China

Abstract

The Rattus norvegicus SILN strain is a common used model for nervous system disorder diseasestudy. We sequenced this R. norvegicus strain SILN mitochondrial genome for the first time(GenBank Accession No. KM114606). Its mitogenome was 16,311 bp and coding 13 protein-coding genes, 2 ribosomal RNA genes, 22 transfer RNA genes.

Keywords

Mitochondrial genome, nervous systemdisorder, Rattus norvegicus

History

Received 9 August 2014Accepted 23 August 2014Published online 3 November 2014

Multiple sclerosis (MS) is an inflammatory demyelinating diseaseof the central nervous system (CNS) that takes a relapsing–remitting or a progressive course (Lassmann et al., 2001; Raine,1997). Its counterpart in the peripheral nervous system (PNS) ischronic inflammatory demyelinating polyradiculoneuropathy(CIDP; Birnbaum & Antel, 1998). In addition, there are acute,monophasic disorders, such as the inflammatory demyelinatingpolyradiculoneuropathy termed Guillain–Barre syndrome (GBS)in the PNS, and acute disseminated encephalomyelitis (ADEM) inthe CNS. Both MS and GBS are heterogeneous syndromes. In MSdifferent exogenous assaults together with genetic factors canresult in a disease course that finally fulfils the diagnostic criteria.In both diseases, axonal damage can add to a primarilydemyelinating lesion and cause permanent neurological deficits.

No single animal model exists that mimics all the features ofhuman demyelinating diseases.

EAE in Rattus norvegicus shares many features with MS inhumans because it can have a chronic, relapsing course and alsoshows histopathological evidence of demyelination (Gold et al.,2000). Both actively induced EAE and AT-EAE can beinvestigated. Susceptible strains such as SILN R. norvegicusexhibit a high degree of heterogeneity in their disease course.With the newer variants of R. norvegicus EAE in mind, the mainadvantage of mouse EAE is that genetically engineered mutantscan be bred. Thus, the influence of genetics on susceptibility,disease course and remyelination can be studied.

Here, we reported complete mitochondrial genome sequenceof a nervous system disorder R. norvegicus SILN strain (Gold

Correspondence: Yun-Liang Wang, Department of Neurology, The 148th Hospital of PLA, Zibo 255300, P.R. China. E-mail: ylwang2211@163.com

Table 1. A list of genes encoded by R. norvegicus mitochondrial genome.

Position Base composition (%)

Gene From To Size (bp) A C G T Start codon Stop codon Strand

tRNAPhe 362 429 67 35.8 25.4 17.9 20.9 H12S rRNA 432 1386 955 36.8 22.7 18.0 22.5 HtRNAVal 1388 1454 67 38.8 19.4 11.9 29.9 H16S rRNA 1455 3024 1570 37.7 21.0 17.7 23.6 HtRNALeu 3025 3099 75 33.3 21.3 16.0 29.4 HND1 3102 4058 957 31.9 27.9 12.6 27.6 ATG TAA HtRNAIle 4058 4126 69 40.6 13.0 14.5 31.9 HtRNAGln 4124 4195 72 25.0 9.7 29.2 36.1 LtRNAMet 4198 4266 69 27.5 24.6 18.9 29.0 HND2 4267 5310 1044 36.4 26.4 8.9 28.3 ATA TAG HtRNATrp 5309 5375 67 37.3 20.9 16.4 25.4 HtRNAAla 5377 5445 69 27.6 10.1 23.2 39.1 LtRNAAsn 5447 5519 73 23.3 16.4 31.5 28.8 L

(continued )

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et al., 2000). We used PCR primers amplification and ABI3730(Applied Biosystems, Foster City, CA) sequencing method to geta complete mitochondrial genome of 16,311 bp long. Sequencefrom the current study was deposited in GenBank (Accession No.KM114606). It included 13 protein-coding genes, 2 rRNA genes,22 tRNA genes and 1 control region (Table 1), which showed asimilar genome structure and gene content with previous reportedR. norvegicus mitochondrial genomes. In this genome, mostprotein-coding genes employed ATG as the start codon besidesND2, ND3 and ND5 initiating with ATA. The overall compositionof the mitogenome was estimated to be 34% for A, 27% for T,26% for C and 13% for G with an A-T (61%)-rich feature. ND6gene was encoded on the L strand, while the others were encodedon the H strand. These genes had four types of stop codon,including TAG for ND2, TAA for eight genes, AGA for CytB, andan incomplete termination codon T– – for COX3, ND3 and ND4.The lengths of 12s rRNA gene and the 16s rRNA gene were953 bp and 1568 bp. This sequence was largely similar to theR. norvegicus strain BN/SsNHsdMCW mitochondrion in gene

order and contents except some single nucleotide polymorphisms(SNPs).

Declaration of interest

The authors report no conflicts of interest. The authors alone areresponsible for the content and writing of the paper.

References

Birnbaum G, Antel J. (1998). Immunology of multiple sclerosis. In: AntelJ, Birnbaum G, Hartung H-P, editors. Clinical neuroimmunology.Oxford: Blackwell’s. p 105–15.

Gold R, Hartung HP, Toyka KV. (2000). Animal models for autoimmunedemyelinating disorders of the nervous system. Mol Med Today 6:88–91.

Lassmann H, Bruck W, Lucchinetti C. (2001). Heterogeneity of multiplesclerosis pathogenesis: implications for diagnosis and therapy. TrendsMol Med 7:115–21.

Raine CS. (1997). Multiple sclerosis clinical and pathogenetic basis.London: Chapman & Hall.

Table 1. Continued

Position Base composition (%)

Gene From To Size (bp) A C G T Start codon Stop codon Strand

OL 5520 5550 31 35.5 29.0 25.8 9.7 LtRNACys 5552 5618 67 25.4 20.9 25.4 28.3 LtRNATyr 5619 5686 68 33.8 16.2 20.6 29.4 LCOX1 5688 7232 1545 28.8 25.3 16.3 29.6 ATG TAA HtRNASer 7230 7298 69 26.1 14.5 27.5 31.9 LtRNAAsp 7306 7373 68 36.8 13.2 17.6 32.4 HCOX2 7375 8058 684 34.2 23.8 14.6 27.4 ATG TAA HtRNALys 8065 8127 63 34.9 17.5 17.5 30.1 HATP8 8130 8330 201 39.8 23.9 7.9 28.4 ATG TAA HATP6 8291 8971 681 33.6 27.4 11.1 27.9 ATG TAA HCOX3 8971 9774 804 26.5 28.7 14.8 30.0 ATG TAG HtRNAGly 9755 9823 69 31.9 18.8 16.0 33.3 HND3 9824 10,180 357 30.3 29.4 12.9 27.4 ATA TAG HtRNAArg 10,171 10,239 69 40.6 10.1 10.1 39.2 HND4L 10,240 10,536 297 32.3 24.6 11.5 31.6 ATG TAA HND4 10,530 11,907 1378 32.3 28.2 10.9 28.6 ATG T– HtRNAHis 11,908 11,977 70 41.4 15.7 8.6 34.3 HtRNASer 11,978 12,037 60 31.7 18.3 16.7 33.3 HtRNALeu 12,039 12,109 71 38.0 14.1 18.3 29.6 HND5 12,110 13,930 1821 32.7 29.3 10.5 27.5 ATA TAA HND6 13,914 14,441 528 22.2 8.7 28.2 40.9 ATG TAA LtRNAGlu 14,442 14,510 69 29.0 11.6 20.3 39.1 LCytB 14,515 15,654 1140 31.2 30.2 13.4 25.2 ATG AGA HtRNAThr 15,658 15,727 70 34.3 21.4 17.1 27.2 HtRNAPro 15,727 15,789 66 24.2 13.7 28.8 33.3 L

2 Y.-Z. Zhang et al. Mitochondrial DNA, Early Online: 1–2

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