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Journal of Bacteriology logoLink to Journal of Bacteriology
. 2012 Oct;194(20):5714–5715. doi: 10.1128/JB.01370-12

Genome Sequence of a Nicotine-Degrading Strain of Arthrobacter

Yuxiang Yao a, Hongzhi Tang a,, Huixue Ren b, Hao Yu a, Lijuan Wang a, Ping Xu a,
PMCID: PMC3458684  PMID: 23012289

Abstract

We announce a 4.63-Mb genome assembly of an isolated bacterium that is the first sequenced nicotine-degrading Arthrobacter strain. Nicotine catabolism genes of the nicotine-degrading plasmid pAO1 were predicted, but plasmid function genes were not found. These results will help to better illustrate the molecular mechanism of nicotine degradation by Arthrobacter.

GENOME ANNOUNCEMENT

Nicotine, as a chemical in the U.S. Environmental Protection Agency's “Toxics Release Inventory” (8), exists abundantly in tobacco waste (3). Microbiological degradation of nicotine is a potential method of tobacco waste treatment. Arthrobacter is one of the two dominant organisms capable of nicotine degradation (2). A new nicotine-degrading strain, Arthrobacter sp. strain M2012083, was isolated from tobacco waste, identified, and deposited at the China Center for Type Culture Collection (CCTCC M2012083). It can efficiently degrade nicotine; use nicotine as its sole carbon, nitrogen, and energy source; and generate blue pigments during nicotine degradation (data not shown). This characteristic is similar to that of well-reported Arthrobacter nicotinovorans pAO1 (2). A 165-kb nicotine-degrading plasmid from A. nicotinovorans, pAO1, has been sequenced (5); with it, the Arthrobacter strain degrades nicotine through the pyridine pathway. However, none of the genomes of nicotine-degrading Arthrobacter species have been sequenced or announced so far.

The draft genome sequence of Arthrobacter sp. strain M2012083 was obtained by Illumina High-Seq 2000 paired-end sequencing (15,210,232 reads, ∼329-fold coverage), and de novo assembly was performed by using the Velvet software, version 1.2.03 (14). The sequence has 67 large contigs (>500 bp) with an N50 length of 139,956 bp. These contigs were analyzed in the Clusters of Orthologous Groups and KEGG databases to predict gene functions and metabolic networks (6). Annotation was performed by the RAST server (1) and the NCBI Prokaryotic Genomes Automatic Annotation Pipeline (9). The 4,629,172-bp draft genome sequence has a GC content of 62.0%, containing 54 tRNA genes and 4,312 predicted coding sequences (CDSs) with a 949-bp average length and an 88.4% coding density. It also contains 387 subsystems comprising 2,576 CDSs in total.

The search revealed a 69-kb sequence with homology to plasmid pAO1 (5). The GC content is about 57.9%, much lower than that of the genome (62.0%). All of the putative nicotine catabolism-related genes of plasmid pAO1 identified were contained in the sequence (4). However, the transposase genes of IS1473, supposed to be the end of the nicotine catabolic transposon (4), were not complete, and the plasmid function genes of pAO1 were not found (4). According to the genomic annotation, both Gram-negative and -positive cell wall components are included in the subsystems (1), in agreement with the typical morphological diversity of these bacteria (7). There are 522 proteins involved in carbohydrate metabolism and 59 proteins involved in the metabolism of aromatic compounds in the subsystems (1). Additionally, the genome carries 89 genes involved in stress responses (1). All of these contribute to the survival ability and competitiveness of Arthrobacter sp. strain M2012083. However, motility genes are absent from this bacterium, which suggests that the strain's competitiveness does not require movement (1). Also, the Pseudomonas nicotine degradation-related genes were not found (1013). This information about the genome of strain M2012083 will help in the study of the molecular mechanism of nicotine degradation by Arthrobacter.

Nucleotide sequence accession numbers.

This whole-genome shotgun project has been deposited at DDBJ/EMBL/GenBank under accession number AKKK00000000. The version described in this paper is the first version, AKKK01000000.

ACKNOWLEDGMENTS

We acknowledge Huajun Zheng for genome sequencing and analysis at the Chinese National Human Genome Center at Shanghai.

This work was supported in part by grants from the Chinese National Natural Science Foundation (30900042 and 30821005) and by the National Basic Research Program of China (2009CB118906). We also acknowledge the Chen Guang project from the Shanghai Municipal Education Commission and the Shanghai Education Development Foundation (10CG10) and the Chen Xing project from Shanghai Jiaotong University.

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