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IntroductionGallibacterium anatis causes gallibacteriosis in birds. These bacteria produce biofilms and secrete several fimbrial appendages as tools to cause disease in animals. G. anatis strains contain up to three types of fimbriae. Complete genome sequencing is the strategy currently used to determine variations in the gene content of G. anatis, although today only the completely circularized genome of G. anatis UMN179 is available.MethodsThe appearance of growth of various strains of G. anatis in liquid culture medium was studied. Biofilm production and how the amount of biofilm was affected by DNase, Proteinase K, and Pronase E enzymes were analyzed. Fimbrial gene expression was performed by protein analysis and qRT-PCR. In an avian model, the pathogenesis generated by the strains G. anatis ESV200 and 12656-12 was investigated. Using bioinformatic tools, the complete genome of G. anatis ESV200 was comparatively studied to search for virulence factors that would help explain the pathogenic behavior of this strain.Results and DiscussionG. anatis ESV200 strain differs from the 12656-12 strain because it produces a biofilm at 20%. G. anatis ESV200 strain express fimbrial genes and produces biofilm but with a different structure than that observed for strain 12656-12. ESV200 and 12656-12 strains are pathogenic for chickens, although the latter is the most virulent. Here, we show that the complete genome of the ESV200 strain is similar to that of the UNM179 strain. However, these strains have evolved with many structural rearrangements; the most striking chromosomal arrangement is a Maverick-like element present in the ESV200 strain.

Supplementary material 1: individual patient data from the discovery cohort. Supplementary material 2: supplementary results; table S1: Prevalence of MGMT promoter methylation and MGMT variants patients from the Discovery cohort; table S2: Multivariate Cox regression model for overall survival (OS) in patients from the discovery cohort that received chemotherapy; table S3: Multivariate Cox regression model for OS, including MGMT variants or promoter methylation in patients from the discovery cohort that did not receive chemotherapy; table S4: Multivariate Cox regression model for progression-free survival (PFS), including MGMT variants or promoter methylation and TP53 variants in patients from the discovery cohort that received chemotherapy; table S5: Multivariate Cox regression model for PFS, including MGMT variants or promoter methylation in patients from the discovery cohort that did not receive chemotherapy; table S6: Multivariate Cox regression model for PFS, including AGT variants and MGMT variants or promoter methylation in patients from the discovery cohort; table S7: Validation cohort multivariate Cox regression model. Supplementary material 3: details and annotations of variants detected in the discovery cohort. Supplementary material 4: clinical data of patients from the validation cohort (TCGA). Supplementary material 5: Annotation of AGT, MGMT and TP53 variants from the validation cohort. Supplementary material 6: REMARK checklist for this work. Supplementary material 7: supplementary methods; Primers used in MGMT gene promoter methylation status assessment.

Doctorado en Ciencias Biomédicas Universidad Nacional Autónoma de México. Posgrado en Ciencias Biomédicas

tesis que para obtener el grado de Doctor en Ciencias Biomédicas, presenta Felipe Vaca Paniagua ; asesor Abraham Landa Piedra. 54, [15] páginas : ilustraciones. Doctorado en Ciencias Biomédicas UNAM, Facultad de Medicina, 2009