This "arrow of time" in the collective change of gene expression across multiple stable gene expression patterns (attractors) is not explained by the regulated activation, the suppression of individual genes which are bidirectional molecular processes, or by the standard dynamical models of the underlying gene circuit which only account for local stability of attractors.
We hypothesize that physiological differences (including insulin sensitivity [SI]) between CAs and AAs can be explained by co-regulated gene networks in tissues involved in glucose homeostasis.
In conclusion, this study demonstrated that prevascularized TEBG by insertion of vascular bundle could significantly promote the new bone regeneration and vascularization compared to non-vascularized TEBG, which could be partially explained by the up-regulated expression of VEGF.
Further analysis revealed that the enhanced activities of SOD and CAT could be largely explained by the up-regulated expression of Cu/Zn SOD, Fe SOD, and CAT in P1L (Fig. 7).
This effect can be explained by the androgen-regulated expression level of prostein that may directly influence the density of the respective HLA class I peptide complex on the surface of the LNCaP 1740 cells.
This could be explained by the expression of QS-regulated resistance traits in densely populated biofilms and floating cell aggregations, or alternatively, by a pleiotropic cost of cheating where less resistant cheats are selectively removed from biofilms.
These data can be explained by assuming that the frequently regulated genes display a "promiscuous" behavior and co-occur in regulated gene lists with different genes in different conditions.
In contrast, the production of another bvg-regulated virulence factor, Prn, was slightly suppressed in ptxP3 strains compared with ptxP1 strains (factor 0.94), indicating that increased Ptx production cannot be explained by a global up-regulation of virulence genes.
We observe a bias towards overall down-regulation of genes in Early versus Late tissues (approximately five times more genes are significantly down-regulated than up-regulated) that cannot be explained by read bias in the respective samples.
These findings might be explained by the presence of additional ICSBP-regulated molecules other than Snail, working on ELP, such as Slug and Twist (Supplementary Figure S8).
