Additional file 3: Figure S1. of Adaptive genomic evolution of opsins reveals that early mammals flourished in nocturnal environments

Species-specific evolutionary rate for mammalian opsins. ω-lineages were standardized subtracting the median and divided by the interquartile range. Coloured circles correspond to the species subjected to branch selection tests and significant results are indicated with an asterisk (*). (PDF 501 kb

Additional file 4: Table S3. of Adaptive genomic evolution of opsins reveals that early mammals flourished in nocturnal environments

Species-specific branch selection tests. The one-ratio model (H0) was tested against the two-ratios model considering the alternative hypotheses (H1) of verifying differentiated ω-ratio in the indicated branch. lnL is the logarithm of the model likelihood and the LRT is the likelihood ratio test. All the LRT comparisons were performed with 1 degree of freedom. Significant alternative hypothesis are marked with an asterisk (*) considering a Bonferroni corrected p-value of 0.002 (24 test comparisons). (PDF 278 kb

Additional file 10: Table S7. of Adaptive genomic evolution of opsins reveals that early mammals flourished in nocturnal environments

Dataset of the eco-morphological variables for the studied mammalian species. Variables: activity pattern (nocturnal, cathemeral and diurnal), VS and UVS OPN1sw1 sensitivity, orbit convergence (degrees, °) and visual acuity (cycle per degree, cpd). OPN1sw1 inactive copies were indicated with an asterisk (*) in the column of the sw1 86 site. Data retrieved from the references [5, 11, 65–72]. (XLSX 22 kb

Additional file 16: Table S12. of Bone-associated gene evolution and the origin of flight in birds

Covariance between dS, ω (dN/dS), gc content, and the three body mass measures (minimum, maximum and average) in 39 mammalian genomes using gene-based tree. The upper triangle shows the values obtained for all mammals and the lower triangle excluding bats. Each cell represent the covariance values and posterior probability are the bracketed values, posterior probability (** - < = 0.025 or > =0.975; * - < =0.05 or > =0.95) are highlighted in bold for the statistically significant correlations. (DOC 35 kb

Additional file 14: Figure S4. of Bone-associated gene evolution and the origin of flight in birds

Body mass association with ω (dN/dS). Avian cladogram showing from CoEvol, the labels are the estimated ω (minimum maximum) for each branch on top and the estimated weight (minimum maximum). (DOC 423 kb

Additional file 15: Table S11. of Bone-associated gene evolution and the origin of flight in birds

Covariance between dS, ω (dN/dS), gc content, and the three body mass measures (minimum, maximum and average) in 45 bird genomes using gene-based tree. The upper triangle shows the values obtained for all birds and the lower triangle excluding flightless birds. Each cell represent the covariance values and posterior probability are the bracketed values, posterior probability (** - < = 0.025 or > =0.975; * - < =0.05 or > =0.95) are highlighted in bold for the statistically significant correlations. (DOC 35 kb

Image_2_IL11-mediated stromal cell activation may not be the master regulator of pro-fibrotic signaling downstream of TGFβ.tif

Fibrotic diseases, such as idiopathic pulmonary fibrosis (IPF) and systemic scleroderma (SSc), are commonly associated with high morbidity and mortality, thereby representing a significant unmet medical need. Interleukin 11 (IL11)-mediated cell activation has been identified as a central mechanism for promoting fibrosis downstream of TGFβ. IL11 signaling has recently been reported to promote fibroblast-to-myofibroblast transition, thus leading to various pro-fibrotic phenotypic changes. We confirmed increased mRNA expression of IL11 and IL11Rα in fibrotic diseases by OMICs approaches and in situ hybridization. However, the vital role of IL11 as a driver for fibrosis was not recapitulated. While induction of IL11 secretion was observed downstream of TGFβ signaling in human lung fibroblasts and epithelial cells, the cellular responses induced by IL11 was quantitatively and qualitatively inferior to that of TGFβ at the transcriptional and translational levels. IL11 blocking antibodies inhibited IL11Rα-proximal STAT3 activation but failed to block TGFβ-induced profibrotic signals. In summary, our results challenge the concept of IL11 blockade as a strategy for providing transformative treatment for fibrosis.</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

DataSheet_1_IL11-mediated stromal cell activation may not be the master regulator of pro-fibrotic signaling downstream of TGFβ.pdf

Fibrotic diseases, such as idiopathic pulmonary fibrosis (IPF) and systemic scleroderma (SSc), are commonly associated with high morbidity and mortality, thereby representing a significant unmet medical need. Interleukin 11 (IL11)-mediated cell activation has been identified as a central mechanism for promoting fibrosis downstream of TGFβ. IL11 signaling has recently been reported to promote fibroblast-to-myofibroblast transition, thus leading to various pro-fibrotic phenotypic changes. We confirmed increased mRNA expression of IL11 and IL11Rα in fibrotic diseases by OMICs approaches and in situ hybridization. However, the vital role of IL11 as a driver for fibrosis was not recapitulated. While induction of IL11 secretion was observed downstream of TGFβ signaling in human lung fibroblasts and epithelial cells, the cellular responses induced by IL11 was quantitatively and qualitatively inferior to that of TGFβ at the transcriptional and translational levels. IL11 blocking antibodies inhibited IL11Rα-proximal STAT3 activation but failed to block TGFβ-induced profibrotic signals. In summary, our results challenge the concept of IL11 blockade as a strategy for providing transformative treatment for fibrosis.</p

DataSheet_2_IL11-mediated stromal cell activation may not be the master regulator of pro-fibrotic signaling downstream of TGFβ.csv

Fibrotic diseases, such as idiopathic pulmonary fibrosis (IPF) and systemic scleroderma (SSc), are commonly associated with high morbidity and mortality, thereby representing a significant unmet medical need. Interleukin 11 (IL11)-mediated cell activation has been identified as a central mechanism for promoting fibrosis downstream of TGFβ. IL11 signaling has recently been reported to promote fibroblast-to-myofibroblast transition, thus leading to various pro-fibrotic phenotypic changes. We confirmed increased mRNA expression of IL11 and IL11Rα in fibrotic diseases by OMICs approaches and in situ hybridization. However, the vital role of IL11 as a driver for fibrosis was not recapitulated. While induction of IL11 secretion was observed downstream of TGFβ signaling in human lung fibroblasts and epithelial cells, the cellular responses induced by IL11 was quantitatively and qualitatively inferior to that of TGFβ at the transcriptional and translational levels. IL11 blocking antibodies inhibited IL11Rα-proximal STAT3 activation but failed to block TGFβ-induced profibrotic signals. In summary, our results challenge the concept of IL11 blockade as a strategy for providing transformative treatment for fibrosis.</p