Project description:Birds and other reptiles possess a diversity of feather and scale-like skin appendages. Feathers are commonly assumed to have originated from ancestral scales in theropod dinosaurs. However, most birds also have scaled feet, indicating birds evolved the capacity to grow both ancestral and derived morphologies. This suggests a more complex evolutionary history than a simple linear transition between feathers and scales. We set out to investigate the evolution of feathers via the comparison of transcriptomes assembled from diverse skin appendages in chicken, emu, and alligator. Our data reveal that feathers and the overlapping ‘scutate’ scales of birds share more similar gene expression to each other, and to two types of alligator scales, than they do to the tuberculate ‘reticulate’ scales on bird footpads. Accordingly, we propose a history of skin appendage diversification, in which feathers and bird scutate scales arose from ancestral archosaur body scales, whereas reticulate scales arose earlier in tetrapod evolution. We also show that many “feather-specific genes” are also expressed in alligator scales. In-situ hybridization results in feather buds suggest that these genes represent ancestral scale genes that acquired novel roles in feather morphogenesis and were repressed in bird scales. Our findings suggest that the differential reuse, in feathers, and suppression, in bird scales, of genes ancestrally expressed in archosaur scales has been a key factor in the origin of feathers – and may represent an important mechanism for the origin of evolutionary novelties.
Project description:Determination of the RNA interacting with vfr mRNA at two different time-points during growth on the three strains PAO1, PA14 and IHMA87, representing the three major P. aeruginosa phylogenetic lineages, using rGRIL-seq.
Project description:Light is the primary environmental cue in resetting the phase of circadian pacemaker in vertebrates. In birds, the effect of light is partly mediated by modulating the levels of circadian genes in the pineal gland. To further elucidate the mechanism by which light resets the circadian clock, we studied gene expression in the chicken pineal gland under acutely extended light period. Three paradigms of treatments were used in this study. For each paradigm, chicks were assigned at random to control treatment (control groups) or light treatment (light groups). All birds in control groups were given 12 h light and 12 h dark period (LD 12:12). Light-on time is referred to as Zeitgeber Time 0 (ZT0). In paradigm 1, birds in the light group (n =25 for each of the groups in each paradigm) were acclimated to LD 12:12 for one week in the same light scheme as were the control birds, then exposed to light for 2 h during the subjective late night (ZT22 to ZT24) on the last day. All birds (including the controls) were sacrificed at ZT0. Pineal glands were dissected and 5-6 pineal glands were pooled for the preparation of one RNA sample. In paradigm 2, birds in the light group were acclimated as in paradigm 1 for one week, then exposed to light for 2 h during the early subjective night (ZT12 to ZT14) on the last day. All birds (including controls) were sacrificed at ZT14. The pineal glands were also pooled as before. In paradigm 3, birds in the light group (n = 25) were kept in LD 15:9 cycle all the time, and all birds (including controls) were sacrificed at ZT14. Similarly, 5-6 pineal glands in the same treatment were pooled.
Project description:Transcriptional profiling was carried out on lung and ileum samples at 1dpi and 3dpi from chickens infected with either low pathogenic (H5N2) or highly pathogenic (H5N1) avian influenza. Infected birds were compared to control birds at each time point.
Project description:Transcriptional profiling was carried out on lung and ileum samples at 1dpi and 3dpi from ducks infected with either low pathogenic (H5N2) or highly pathogenic (H5N1) avian influenza. Infected birds were compared to control birds at each time point.
Project description:Transcriptional profiling was carried out on lung and ileum samples at 1dpi and 3dpi from quail infected with either low pathogenic (H5N2) or highly pathogenic (H5N1) avian influenza. Infected birds were compared to control birds at each time point.