Transcriptomic analysis of OsRUS1 overexpression rice lines with rapid and dynamic leaf rolling morphology
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA529208 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR8787304_1.fastq.gz | Fastqsanger.gz | |||
| SRR8787304_2.fastq.gz | Fastqsanger.gz | |||
| SRR8787305_1.fastq.gz | Fastqsanger.gz | |||
| SRR8787305_2.fastq.gz | Fastqsanger.gz | |||
| SRR8787306_1.fastq.gz | Fastqsanger.gz |
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Project description:OsRUS1-GFP overexpression (OsRUS1-OX) transgenic rice lines were generated using ZH-11 wildtype. Under well-watered conditions, the leaves of OsRUS1-OX transgenic rice lines could roll in about four minutes under sunlight, and the rolled leaves of OsRUS1-OX transgenic rice lines could expand in about seven minutes if the sunlight was shaded, while the leaves of wildtype ZH-11 expanded all the times at the same conditions. The mechanism behind the light-responded rapid and dynamic leaf rolling phenotype of OsRUS1-OX transgenic rice lines is unknown. Therefore, in order to understand this mechanism the RNA-Seq approach was used to explore the expressed genes difference between OsRUS1-OX and ZH-11.
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Project description:Leaf rolling and discoloration are two chilling injury symptoms that are widely adopted as indicators for evaluation of cold tolerance at the seedling stage in rice, respectively. However, their relationship has not been well investigated, in particular the mechanism on how low temperature causes leaf rolling at a genome-wide level. In this study, a cold-tolerant japonica cultivar Lijiangxintuanheigu and a cold-sensitive indica cultivar Sanhuangzhan-2 were subjected to different low temperature treatments and physiological and genome-wide gene expression analysis were conducted. Our results showed that leaf rolling happened at temperatures lower than 11℃, but discoloration appeared at moderately low temperatures, such as 13℃. Chlorophyll contents of the two cultivars significantly decreased under 13℃, but didn’t change under 11℃. Contrastly, their relative water contents and the relative electrolyte leakages decreased significantly. Genome-wide gene expression profiling of LTH revealed that the calcium signaling related genes and the genes related to ABA degradation significantly changed under 11℃. Moreover, numerous genes in DREB, MYB, bZIP, NAC, Zin finger, bHLH, WRKY gene families were differently expressed. Furthermore, many aquaporin genes, the key genes in trehalose and starch synthesis were down-regulated under 11℃. These results suggest that the two chilling injury symptoms are controlled by different mechanisms. Cold-induced leaf rolling is associated with calcium and ABA signaling pathways, and subjected to regulation of multiple transcription regulators. The suppression of aquaporin genes and reduced accumulation of soluble sugars under cold stress result in reduction of water potential in cells and consequently, leaf rolling.
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Project description:Proinflammatory stimuli rapidly and globally remodel chromatin landscape, thereby enabling transcriptional responses. Yet, the mechanisms coupling chromatin regulators to the master regulatory inflammatory transcription factor NF-kB remain poorly understood. We report in human endothelial cells (ECs) that activated NF-kB binds to enhancers, provoking a rapid, global redistribution of BRD4 preferentially at super-enhancers, large enhancer domains highly bound by chromatin regulators. Newly established NF-kB super-enhancers drive nearby canonical inflammatory response genes. In both ECs and macrophages BET bromodomain inhibition prevents super-enhancer formation downstream of NF-kB activation, abrogating proinflammatory transcription. In TNFa-activated endothelium this culminates in functional suppression of leukocyte rolling, adhesion and transmigration. Sustained BET bromodomain inhibitor treatment of LDLr -/- animals suppresses atherogenesis, a disease process rooted in pathological vascular inflammation involving endothelium and macrophages. These data establish BET-bromodomains as key effectors of inflammatory response through their role in the dynamic, global reorganization of super-enhancers during NF-kB activation. Gene expression analysis of human endothelial cells in resting state, treatment with TNFalpha or TNFalpha with the BET bromodomain inhibitor JQ1
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Project description:Proinflammatory stimuli rapidly and globally remodel chromatin landscape, thereby enabling transcriptional responses. Yet, the mechanisms coupling chromatin regulators to the master regulatory inflammatory transcription factor NF-kB remain poorly understood. We report in human endothelial cells (ECs) that activated NF-kB binds to enhancers, provoking a rapid, global redistribution of BRD4 preferentially at super-enhancers, large enhancer domains highly bound by chromatin regulators. Newly established NF-kB super-enhancers drive nearby canonical inflammatory response genes. In both ECs and macrophages BET bromodomain inhibition prevents super-enhancer formation downstream of NF-kB activation, abrogating proinflammatory transcription. In TNFa-activated endothelium this culminates in functional suppression of leukocyte rolling, adhesion and transmigration. Sustained BET bromodomain inhibitor treatment of LDLr -/- animals suppresses atherogenesis, a disease process rooted in pathological vascular inflammation involving endothelium and macrophages. These data establish BET-bromodomains as key effectors of inflammatory response through their role in the dynamic, global reorganization of super-enhancers during NF-kB activation.
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Project description:Proinflammatory stimuli rapidly and globally remodel chromatin landscape, thereby enabling transcriptional responses. Yet, the mechanisms coupling chromatin regulators to the master regulatory inflammatory transcription factor NF-kB remain poorly understood. We report in human endothelial cells (ECs) that activated NF-kB binds to enhancers, provoking a rapid, global redistribution of BRD4 preferentially at super-enhancers, large enhancer domains highly bound by chromatin regulators. Newly established NF-kB super-enhancers drive nearby canonical inflammatory response genes. In both ECs and macrophages BET bromodomain inhibition prevents super-enhancer formation downstream of NF-kB activation, abrogating proinflammatory transcription. In TNFa-activated endothelium this culminates in functional suppression of leukocyte rolling, adhesion and transmigration. Sustained BET bromodomain inhibitor treatment of LDLr -/- animals suppresses atherogenesis, a disease process rooted in pathological vascular inflammation involving endothelium and macrophages. These data establish BET-bromodomains as key effectors of inflammatory response through their role in the dynamic, global reorganization of super-enhancers during NF-kB activation.
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