Emu (Dromaius novaehollandiae) and Chicken
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA311140 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR5515050_1.fastq.gz | Fastqsanger.gz | |||
| SRR5515050_2.fastq.gz | Fastqsanger.gz | |||
| SRR5518880_1.fastq.gz | Fastqsanger.gz | |||
| SRR5518880_2.fastq.gz | Fastqsanger.gz | |||
| SRR5518881_1.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 28 |
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Project description:The evolutionary origin of powered flight was fundamental to the establishment and radiation of the avian clade, and it remains a salient feature of modern birds. However, flight has been lost multiple times throughout the evolution of the avian lineage. Ratites (flightless palaeognaths, including the emu, ostrich and other well-known groups) are perhaps the most notable flightless birds, and their convergent losses of flight often coincide with adaptations to a cursorial lifestyle, including robust legs, digit loss, and reduced wings. Although there is a wealth of comparative anatomical knowledge for several ratites, the underlying genetic mechanisms producing these changes remain debated. Here we use a multidisciplinary approach employing embryological, genetic, and genomic techniques to interrogate the mechanisms underlying the delay in forelimb development contributing to the diminution of the forelimb in emu embryos. We show that the epithelial to mesenchymal transition (EMT) in the lateral plate mesoderm (LPM) and muscle precursor migration, the initiating events of limb formation, occur at equivalent stages in the emu and chick. However, the early emu forelimb fails to proliferate at HH18. The unique emu forelimb expression of Nkx2.5, previously associated with diminished wing development, does not initiate until after this stage, concomitant with migration of myoblasts into the limb bud, and hence would not appear to be the proximal cause of limb reduction in this species. In contrast, RNA-sequencing of HH18 limb tissues reveals significantly lower Fgf10 expression in the emu forelimb. Artificially increasing mesenchymal Fgf10 expression to the nascent emu wing induces ectodermal Fgf8 expression and results in a proliferative limb bud. Analyzing open chromatin reveals differentially active regulatory elements near Fgf10 and Sall-1 in the emu wing compared to emu hindlimb and both chicken limbs. Additionally, we show that the Sall-1 enhancer activity is dependent on an Ets transcription factor-binding site likely mediated by Fgf-signaling. Taken together, our results support a model where regulatory changes result in lower expression of Fgf10 and a concomitant failure to induce the genes required for limb proliferation in the early emu wing bud at HH18.
2019-09-30 | GSE136775 | GEO
Project description:The evolutionary origin of powered flight was fundamental to the establishment and radiation of the avian clade, and it remains a salient feature of modern birds. However, flight has been lost multiple times throughout the evolution of the avian lineage. Ratites (flightless palaeognaths, including the emu, ostrich and other well-known groups) are perhaps the most notable flightless birds, and their convergent losses of flight often coincide with adaptations to a cursorial lifestyle, including robust legs, digit loss, and reduced wings. Although there is a wealth of comparative anatomical knowledge for several ratites, the underlying genetic mechanisms producing these changes remain debated. Here we use a multidisciplinary approach employing embryological, genetic, and genomic techniques to interrogate the mechanisms underlying the delay in forelimb development contributing to the diminution of the forelimb in emu embryos. We show that the epithelial to mesenchymal transition (EMT) in the lateral plate mesoderm (LPM) and muscle precursor migration, the initiating events of limb formation, occur at equivalent stages in the emu and chick. However, the early emu forelimb fails to proliferate at HH18. The unique emu forelimb expression of Nkx2.5, previously associated with diminished wing development, does not initiate until after this stage, concomitant with migration of myoblasts into the limb bud, and hence would not appear to be the proximal cause of limb reduction in this species. In contrast, RNA-sequencing of HH18 limb tissues reveals significantly lower Fgf10 expression in the emu forelimb. Artificially increasing mesenchymal Fgf10 expression to the nascent emu wing induces ectodermal Fgf8 expression and results in a proliferative limb bud. Analyzing open chromatin reveals differentially active regulatory elements near Fgf10 and Sall-1 in the emu wing compared to emu hindlimb and both chicken limbs. Additionally, we show that the Sall-1 enhancer activity is dependent on an Ets transcription factor-binding site likely mediated by Fgf-signaling. Taken together, our results support a model where regulatory changes result in lower expression of Fgf10 and a concomitant failure to induce the genes required for limb proliferation in the early emu wing bud at HH18.
2019-09-30 | GSE136774 | GEO
Project description:Dromaius novaehollandiae (Emu) Transcriptome profiling
| PRJNA511938 | ENA
Project description:Powered flight was fundamental to the establishment and radiation of birds. However, flight has been lost multiple times throughout avian evolution. Convergent losses of flight within the ratites (flightless paleognaths, including the emu and ostrich) often coincide with reduced wings. Although there is a wealth of anatomical knowledge for several ratites, the genetic mechanisms causing these changes remain debated. Here, we use a multidisciplinary approach employing embryological, genetic, and genomic techniques to interrogate the mechanisms underlying forelimb heterochrony in emu embryos. We show that the initiation of limb formation, an epithelial to mesenchymal transition (EMT) in the lateral plate mesoderm (LPM) and myoblast migration into the LPM, occur at equivalent stages in the emu and chick. However, the emu forelimb fails to subsequently proliferate. The unique emu forelimb expression of Nkx2.5, previously associated with diminished wing development, initiates after this stage (concomitant with myoblast migration into the LPM) and is therefore unlikely to cause this developmental delay. In contrast, RNA sequencing of limb tissue reveals significantly lower Fgf10 expression in the emu forelimb. Artificially increasing Fgf10 expression in the emu LPM induces ectodermal Fgf8 expression and a limb bud. Analyzing open chromatin reveals differentially active regulatory elements near Fgf10 and Sall-1 in the emu wing, and the Sall-1 enhancer activity is dependent on a likely Fgf-mediated Ets transcription factor-binding site. Taken together, our results suggest that regulatory changes result in lower expression of Fgf10 and a concomitant failure to express genes required for limb proliferation in the early emu wing bud.
| S-EPMC6834345 | biostudies-literature
Project description:Emu (Dromaius novaehollandiae) farming has been gaining wide interest for fat production. Oil rendered from this large flightless bird's fat is valued for its anti-inflammatory and antioxidant properties for uses in therapeutics and cosmetics. We analyzed the seasonal and sex-dependent differentially expressed (DE) genes involved in fat metabolism in emus. Samples were taken from back and abdominal fat tissues of a single set of four male and four female emus in April, June, and November for RNA-sequencing. We found 100 DE genes (47 seasonally in males; 34 seasonally in females; 19 between sexes). Seasonally DE genes with significant difference between the sexes in gene ontology terms suggested integrin beta chain-2 (ITGB2) influences fat changes, in concordance with earlier studies. Six seasonally DE genes functioned in more than two enriched pathways (two female: angiopoietin-like 4 (ANGPTL4) and lipoprotein lipase (LPL); four male: lumican (LUM), osteoglycin (OGN), aldolase B (ALDOB), and solute carrier family 37 member 2 (SLC37A2)). Two sexually DE genes, follicle stimulating hormone receptor (FSHR) and perilipin 2 (PLIN2), had functional investigations supporting their influence on fat gain and loss. The results suggested these nine genes influence fat metabolism and deposition in emus.
| S-EPMC9177602 | biostudies-literature
Project description:The emu is a large, (bipedal) flightless bird that potentially can be used to study various orthopaedic disorders in which load protection of the experimental limb is a limitation of quadrupedal models. An anatomy-based analysis of normal emu walking gait was undertaken to determine hip contact forces for comparison with human data. Kinematic and kinetic data captured for two laboratory-habituated emus were used to drive the model. Muscle attachment data were obtained by dissection, and bony geometries were obtained by CT scan. Inverse dynamics calculations at all major lower-limb joints were used in conjunction with optimization of muscle forces to determine hip contact forces. Like human walking gait, emu ground reaction forces showed a bimodal distribution over the course of the stance phase. Two-bird averaged maximum hip contact force was approximately 5.5 times body weight, directed nominally axially along the femur. This value is only modestly larger than optimization-based hip contact forces reported in literature for humans. The interspecies similarity in hip contact forces makes the emu a biomechanically attractive animal in which to model loading-dependent human orthopaedic hip disorders.
| S-EPMC2291359 | biostudies-literature
Project description:Characterization of carcass traits and fat quality is important to effectively produce and genetically improve emus. We investigated carcass traits in 309 emus. The meat production of female emus showed a significantly higher value than that of males (P < 0.01). The fat weight of male (9.232 ± 3.156 kg) was larger than that of the female (7.772 ± 2.697 kg). The fat yield (fat weight per kg of body weight) was strongly correlated to body weight (r = 0.79 and r = 0.75 in male and female, respectively). The fat melting points of females and males were 19.19 ± 3.39°C and 19.39 ± 3.39°C, respectively, without significant difference. Since the fat melting point did not correlate to body and fat weights, we predicted that it was an independent trait from body growth and was highly influenced by genetic elements. Percentages of palmitic, stearic, oleic, linoleic, and α-linolenic acids were 22.27 ± 3.50%, 9.37 ± 1.90%, 54.11 ± 5.17%, 13.54 ± 7.80% and 0.71 ± 0.59%, respectively. Among them, linoleic acid contents showed a wide individual difference (range 0.3-19.9%). The oleic/stearic acid ratio showed a negative correlation to the fat melting point. These results suggest that the fat melting point is a good indicator of C18:1/C18:0 ratio in emu fat.
| S-EPMC9385692 | biostudies-literature
Project description:phased assembly of female emu (Alternate Pseudohaplotype)
| PRJDB10283 | ENA
Project description:phased assembly of female emu (Principal Pseudohaplotype)
| PRJDB10282 | ENA