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Background Enterococcus raffinosus is one of the Enterococcus species that often cause nosocomial infections. To date, only one E. raffinosus genome has been completely assembled, and the genomic features have not been characterized. Here, we report the complete genome sequence of the strain CX012922, isolated from the feces of a Crohn’s disease patient, and perform a comparative genome analysis to the relevant Enterococcus spp. strains in silico. Results De novo assembly of the sequencing reads of the strain CX012922 generated a circular genome of 2.83 Mb and a circular megaplasmid of 0.98 Mb. Phylogenomic analysis revealed that the strain CX012922 belonged to the E. raffinosus species. By comparative genome analysis, we found that some strains previously identified as E. raffinosus or E. gilvus should be reclassified as novel species. Genome islands (GIs), virulence factors, and antibiotic genes were found in both the genome and the megaplasmid, although pathogenic genes were mainly encoded in the genome. A large proportion of the genes encoded in the megaplasmid were involved in substrate utilization, such as raffinose metabolism. Giant megaplasmids (~1 Mb) equipped with toxin-antitoxin (TA) systems generally formed symbiosis relationships with the genome of E. raffinosus strains. Conclusions Enterococcus spp. have a higher species-level diversity than is currently appreciated. The pathogenicity of E. raffinosus is mainly determined by the genome-encoded virulence factors, while the megaplasmid broadens the gene function pool. The symbiosis between the genome and the megaplasmids endows E. raffinosus with large genomic sizes as well as versatile gene functions, especially for their colonization, adaptation, virulence, and pathogenesis in the human gut.

BackgroundParaclostridium bifermentans is the most diverse distributed species of Paraclostridium and can cause fatal human infections under rare conditions. However, its pathogenic mechanisms and adaptation ability behind infections remain unclear. Herein, we reported the complete genome sequence of P. bifermentans HD0315_2 isolated from the feces of a patient with Crohn's disease. Then, we performed genomic analyses to understand its pathogenic mechanisms and adaptation ability.ResultsThe de novo assembly revealed that the HD0315_2 strain carried a circular chromosome of 3.27 Mb and six circular plasmids (19.41 to 139.50 kb). The phylogenomic analysis assigned the HD0315_2 strain as P. bifermentans and reclassified some previously non-P. bifermentans strains into this clade. The general genomic features showed that this species harbored a flexible genomic pool characterized by variable genome length and multiple plasmids. Then, the HD0315_2 strain was predicted as a human pathogen with high probability, and Listeria LIPI-1 virulence proteins were identified on its genome. Besides, abundant antibiotics/metal/stress resistant genes, such as asrABCH, cat, mccF, macB, entS, albA, bcrA, and tetB, were carried by either the genome or the plasmids. Furthermore, we proposed that transposase-directed horizontal gene transfer was responsible for the distribution of multiple copies of the hin gene in the plasmids.ConclusionThe flexible genomic pool of P. bifermentans encodes abundant functions for antimicrobial or oxidative stress resistance, helping it successfully inhabit and adapt to diverse environments. Moreover, P. bifermentans HD0315_2 might infect hosts via a Listeria LIPI-1-like cycle, with the help of a plasmid expressing the Hin DNA invertase to evade host immune responses.

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Homeobox genes (HOX genes) have been implicated in many tumors. As a member of HOX genes, HOXB5 is overexpressed in bladder cancer and contributes to the proliferation and invasion of breast cancer cells. However, functions of HOXB5 in retinoblastoma remain elusive. In this study, we found that HOXB5 expression is upregulated in retinoblastoma cell lines and tissues. Overexpression of HOXB5 promoted retinoblastoma cell migration and invasion, but knockdown of HOXB5 suppressed the migration and invasion. Moreover, HOXB5 induced the activation of ERK1/2 and upregulated the production of MMP-3 and MMP-13. In addition, ERK1/2 pathway was required for HOXB5-mediated retinoblastoma cell migration and invasion. Taken together, our study suggests that HOXB5 promotes the migration and invasion of retinoblastoma cells by inducing the activation of ERK1/2 and increasing the production of MMP-3 and MMP-13. Therefore, HOXB5 may represent an effective target for treatment of retinoblastoma.