Project description:We have completed the high quality reference genome for domestic sheep (Oar v3.1) and performed a detailed survey of gene expression across different tissues. RNA-seq data of 7 tissue types from the reference female Texel and skin tissue from a Gansu alpine fine wool sheep were sequenced.
Project description:Abstract: Obesity is a major health concern that lacks effective intervention strategies. Traumatic acid (TA) is a potent wound-healing agent in plants, considered an antioxidant food ingredient. This study demonstrated that TA treatment significantly re-duced lipid accumulation in human adipocytes and prevented high-fat diet (HFD) induced obesity in zebrafish. Transcriptome sequencing revealed TA-activated fatty acid (FA) degradation and FA metabolism signaling pathways. Moreover, western blot-ting and quantitative polymerase chain reaction showed that TA inhibited the expression of long-chain acyl-CoA synthetase-4 (ACSL4). Overexpression of ACSL4 resulted in the reversal of TA beneficiary effects, indicating that the attenuated lipid accu-mulation of TA was regulated by ACSL4 expression. Limited proteolysis-mass spectrometry and microscale thermophoresis were then used to confirm hexokinase 2 (HK2) as a direct molecular target of TA. Thus, we demonstrated the molecular basis of TA in regulating lipid accumulation and gave the first evidence that TA may function through the HK2-ACSL4 axis.
Project description:Despite advances in assisted reproductive technology, success rates remain modest, largely due to implantation failure and inadequate support of early pregnancy. Corpus luteum function and consequent progesterone secretion are essential for these processes. Large luteal cells are the primary source of progesterone production, yet the transcriptional programs that define their identity remain unclear. Here, we identify the nuclear receptor Liver receptor homolog-1 as a key regulator of large luteal cell function. Loss of Liver receptor homolog-1 disrupts lipid droplet accumulation and downregulates key steroidogenic genes. Mechanistically, Liver receptor homolog-1 undergoes chromatin-binding reprogramming during luteinization, establishing regulatory regions that couple lipid metabolism to steroidogenesis. Large luteal cells integrate energy metabolism with steroid hormone production and promote nuclear acetyl-coenzyme A synthesis via Acyl-CoA synthetase short-chain family member 2, linking metabolic reprogramming to epigenetic control. These findings establish Liver receptor homolog-1 and Acyl-CoA synthetase short-chain family member 2 as key regulators coordinating lipid homeostasis, chromatin regulation and fertility.
Project description:Despite advances in assisted reproductive technology, success rates remain modest, largely due to implantation failure and inadequate support of early pregnancy. Corpus luteum function and consequent progesterone secretion are essential for these processes. Large luteal cells are the primary source of progesterone production, yet the transcriptional programs that define their identity remain unclear. Here, we identify the nuclear receptor Liver receptor homolog-1 as a key regulator of large luteal cell function. Loss of Liver receptor homolog-1 disrupts lipid droplet accumulation and downregulates key steroidogenic genes. Mechanistically, Liver receptor homolog-1 undergoes chromatin-binding reprogramming during luteinization, establishing regulatory regions that couple lipid metabolism to steroidogenesis. Large luteal cells integrate energy metabolism with steroid hormone production and promote nuclear acetyl-coenzyme A synthesis via Acyl-CoA synthetase short-chain family member 2, linking metabolic reprogramming to epigenetic control. These findings establish Liver receptor homolog-1 and Acyl-CoA synthetase short-chain family member 2 as key regulators coordinating lipid homeostasis, chromatin regulation and fertility.
Project description:Despite advances in assisted reproductive technology, success rates remain modest, largely due to implantation failure and inadequate support of early pregnancy. Corpus luteum function and consequent progesterone secretion are essential for these processes. Large luteal cells are the primary source of progesterone production, yet the transcriptional programs that define their identity remain unclear. Here, we identify the nuclear receptor Liver receptor homolog-1 as a key regulator of large luteal cell function. Loss of Liver receptor homolog-1 disrupts lipid droplet accumulation and downregulates key steroidogenic genes. Mechanistically, Liver receptor homolog-1 undergoes chromatin-binding reprogramming during luteinization, establishing regulatory regions that couple lipid metabolism to steroidogenesis. Large luteal cells integrate energy metabolism with steroid hormone production and promote nuclear acetyl-coenzyme A synthesis via Acyl-CoA synthetase short-chain family member 2, linking metabolic reprogramming to epigenetic control. These findings establish Liver receptor homolog-1 and Acyl-CoA synthetase short-chain family member 2 as key regulators coordinating lipid homeostasis, chromatin regulation and fertility.
Project description:We have completed the high quality reference genome for domestic sheep (Oar v3.1) and performed a detailed survey of gene expression across different tissues. RNA-seq data of 7 tissue types from the reference female Texel and skin tissue from a Gansu alpine fine wool sheep were sequenced. Here is the part of the RNA-seq data sequenced in BGI, including 7 tissue types from the reference female Texel and skin type from a Gansu alpine fine wool sheep.
Project description:We have completed the high quality reference genome for domestic sheep (Oar v3.1). Early-stage Illumina GA sequence platform sequenced less reads in high GC content regions than in other regions. To read through higher GC content regions, we generated 2 Gb MeDIP-seq data for filling gaps in sheep reference genome assembly.
Project description:We were interested in transcriptional changes after depletion of the lipid metabolic gene Acyl-CoA Synthetase Long Chain Family Member 4 (ACSL4) in human acute myleoid leukemia (AML) cell lines. We compared global alterations of gene expression upon ACSL4 knockdown in one AML cell line harboring a lysine methyltransferase 2A (KMT2A) gene rearrangement (NOMO1) and one KMT2A WT AML cell line (K562).