Phylogenetic reconstruction based on nucleotide sequence of fulllength proviral FIV including and separate analysis of

A. Phylogenetic tree of concatenated combined data of coding genes , , and . B. Phylogenetic tree of sequences only. Shown is the maximum likelihood tree (ML) identical to tree topology using maximum parisimony (MP) and minimum evolution (ME) for each gene region. See methods and Additional file for specific parameters as implemented in PAUP ver 4.10b. All nodes supported by 100% bootstrap proportions in ME, MP and ML analyses except for relative positions of FIVsubtypes which were supported by bootstraps >50% but less than 100% within the FIVclade.<p><b>Copyright information:</b></p><p>Taken from "Genomic organization, sequence divergence, and recombination of feline immunodeficiency virus from lions in the wild"</p><p>http://www.biomedcentral.com/1471-2164/9/66</p><p>BMC Genomics 2008;9():66-66.</p><p>Published online 5 Feb 2008</p><p>PMCID:PMC2270836.</p><p></p

Phylogenetic reconstruction based on nucleotide sequence of LTR and coding genes from full-length FIV nucleotide sequences excluding

(A-E) Shown are the maximum likelihood trees (ML) which are identical to tree topologies using maximum parisimony (MP) and minimum evolution (ME) for each gene region. See methods and Additional file for specific parameters as implemented in PAUP ver 4.10b. (E) phylogeny does not include FIVsubtype A due to lack of sufficient homology for proper gene identification. (F) Phylogenetic tree of concatenated combined data of coding genes , , and . All nodes supported by 100% bootstrap proportions in ME, MP and ML analyses except for relative positions of FIVsubtypes which were supported by bootstraps >50% but less than 100% within the FIVclade.<p><b>Copyright information:</b></p><p>Taken from "Genomic organization, sequence divergence, and recombination of feline immunodeficiency virus from lions in the wild"</p><p>http://www.biomedcentral.com/1471-2164/9/66</p><p>BMC Genomics 2008;9():66-66.</p><p>Published online 5 Feb 2008</p><p>PMCID:PMC2270836.</p><p></p

Additional file 2 of Genomic legacy of the African cheetah, Acinonyx jubatus

Supplemental tables. Table S1. Sequenced cheetah reads for de novo genome assembly. Table S2. Re-sequenced cheetah reads for population analyses. Table S3. Estimated cheetah genome size. Table S4. Cheetah genome assembly information. Table S5. Reference-assisted assembly of cheetah chromosomes. Table S6. RepeatMasker results for transposable elements in carnivore genomes. Table S7. Total length of repeat regions in cheetah. Table S8. Tandem repeats in five carnivore genomes. Table S9. Complex tandem repeat families. Table S10. Protein-coding gene annotation. Table S11. Non-coding RNA annotation. Table S12. Nuclear mitochondrial genes. Table S13. Lengths of cheetah synteny blocks. Table S14. Cheetah rearrangements. Table S15. Called SNV statistics. Table S16. SNV effects by impact. Table S17. SNV effects by functional class. Table S18. SNV effects by genomic region. Table S19. SNV locations relative to genes. Table S20. SNV distribution in cheetah genome. Table S21. SNV distribution in tiger genomes. Table S22. SNV locations and effects in coding genes of Felidae genomes. Table S23. SNV counts in genes in domestic cat and tigers. Table S24. SNV counts in genes in cheetahs. Table S25. Nucleotide diversity in mitochondrial genomes of mammals. Table S26. Nucleotide diversity in MHC class I and II genes. Table S27. Demographic models and their log-likelihood values. Table S28. Population data by DaDi. Table S29. Reproductive system genes with identified function. Table S30. Filtration of cheetah reproduction system genes. Table S31. Nucleotide diversity of masked assemblies. Table S32. Statistics on autosomal segmental duplications. (PDF 127 kb

NY-ESO-1 expression in DCIS: A new predictor of good prognosis

BACKGROUND: At present, it is difficult to predict which patients with ductal carcinoma-in-situ (DCIS) will subsequently develop frank invasive breast cancer (IDC). A recent survey by our group has shown that NY-ESO-1 and MAGEA are both expressed in DCIS. This study was aimed at determining whether expression of these antigens was related to the later development of IDC. RESULTS: 14 of 42 (33%) of patients developed invasive breast cancer during the follow up period. Only one of those DCIS cases that relapsed was positive for NYESO-1 at diagnosis. In contrast, DCIS samples of 15 of the 28 (54%) of those patients who remained disease-free expressed NY-ESO-1. (Permutation chi square p=0.0033). METHODS: We identified 42 patients with DCIS, and followed them up for more than 10 years. NY-ESO-1 and MAGEA were demonstrated by immunostaining as were CD8+ infiltrates on all sections together with the conventional markers, ER, PR, and HER2. CONCLUSIONS: Expression of NY-ESO-1 may predict those patients who will not subsequently develop invasive breast cancer and could therefore potentially be helpful in defining prognosis in patients with DCIS

Additional file 3 of Genomic legacy of the African cheetah, Acinonyx jubatus

Supplemental datasheets. Datasheet S1. List of cheetah-specific de novo predicted genes with functional domains annotated by InterPro scan. Datasheet S2. List of gene families in eight mammal species identified by protein homology. Datasheet S3. Results of gene family expansion and contraction analysis. Datasheet S4. CAFE results from gene family contraction and expansion analysis. Datasheet S5. Results of gene selection analysis. Datasheet S6. Reproductive system genes with damaging mutations. Datasheet S7. Segmental duplication genes. Datasheet S8. List of reproductive genes with segregated high effect mutations and corresponding genotypes of cheetah. (XLSX 711 kb

Additional file 2: Figure S1. of Comparison of carnivore, omnivore, and herbivore mammalian genomes with a new leopard assembly

Species and sub-species identification for three leopard samples. Figure S2. Distribution of K-mer frequency in the error-corrected reads. Figure S3. GC content distributions. Figure S4. Composition of mammalian orthologous genes. Figure S5. Divergence time estimation of 18 mammals. Figure S6. Contraction of the amylase gene families (AMY1 and AMY2) in carnivores. Figure S7. Frame-shift mutations in Felidae GCKR genes. Figure S8. Felidae-specific amino acid changes in DNA repair system. Figure S9. Felidae-specific amino acid change in MEP1A protein. Figure S10. Felidae-specific amino acid change in ACE2 protein. Figure S11. Felidae-specific amino acid change in PRCP protein. (DOCX 2024 kb

Additional file 3: of Comparison of carnivore, omnivore, and herbivore mammalian genomes with a new leopard assembly

Tables S1-50. (DOCX 174 kb

Additional file 2: Figure S1. of Comparison of carnivore, omnivore, and herbivore mammalian genomes with a new leopard assembly

Species and sub-species identification for three leopard samples. Figure S2. Distribution of K-mer frequency in the error-corrected reads. Figure S3. GC content distributions. Figure S4. Composition of mammalian orthologous genes. Figure S5. Divergence time estimation of 18 mammals. Figure S6. Contraction of the amylase gene families (AMY1 and AMY2) in carnivores. Figure S7. Frame-shift mutations in Felidae GCKR genes. Figure S8. Felidae-specific amino acid changes in DNA repair system. Figure S9. Felidae-specific amino acid change in MEP1A protein. Figure S10. Felidae-specific amino acid change in ACE2 protein. Figure S11. Felidae-specific amino acid change in PRCP protein. (DOCX 2024 kb