TEAD1 and TEAD3 play redundant roles in human epidermal proliferation
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA576911 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR10258850.fastq.gz | Fastqsanger.gz | |||
| SRR10258851.fastq.gz | Fastqsanger.gz | |||
| SRR10258852.fastq.gz | Fastqsanger.gz |
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Project description:Our previous study on CBP60g, a calmodulin binding protein that is important for disease resistance and microbe-associated molecular pattern (MAMP)-induced SA accumulation, led to our discovery of a closely related family member CBP60h. CBP60h is also important for defense against P. syringae but is induced differently by pathogen and MAMP stimulus. Transcriptome profiling of cbp60h mutants suggested that CBP60h might be primarily functioning in response against P. syringae. We constructed a double mutant of cbp60g and cbp60h, which demonstrated severely defective defense against P. syringae and SA accumulation. Profiling of the cbp60g/h showed that its expression pattern is very similar to that of pad4. Transient expression in Tobacco showed that both CBP60g and CBP60h localized to nucleus. Our observation suggest that CBP60g and CBP60h share partially redundant but critical role in defense response and SA signaling. This experiment consists of three biological replicates. For each genotype, two leaves per plant were pooled from three pots to prepare total RNA.
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Project description:Defining the function of TEAD transcription factors in myogenic differentiation has proved elusive due to overlapping expression and functional redundancy. Here, we show that siRNA silencing of either Tead1, Tead2 or Tead4 did not effect differentiation of primary myoblasts (PMs) while their simultaneous knockdown strongly impaired differentiation. In contrast in C2C12 cells, silencing of Tead1 or Tead4 impaired differentiation showing a differential requirement for these factors in PMs and C2C12 cells that involved both differential regulation of their expression and intracellular localisation. Through integration of Tead1 and Tead4 ChIP-seq with chromatin modifications, we identify active enhancers associated with genes activated during C2C12 cell differentiation that are bound by combinations of Tead4, Myod1 or Myog and show a signature of frequently co-occuring motifs. We show that distinct but overlapping sets of genes are deregulated by Tead silencing in C2C12 cells and PMs therefore describing for the first time in a comprehensive manner the specific and redundant regulatory roles of Tead factors in myogenic differentiation. We also performed ChIP-seq from mouse muscle in vivo identifying a set of highly transcribed muscle cell-identity genes and revealing that Tead4 binds a distinct repertoire of sites in C2C12 cells and muscle.
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Project description:Defining the function of TEAD transcription factors in myogenic differentiation has proved elusive due to overlapping expression and functional redundancy. Here, we show that siRNA silencing of either Tead1, Tead2 or Tead4 did not effect differentiation of primary myoblasts (PMs) while their simultaneous knockdown strongly impaired differentiation. In contrast in C2C12 cells, silencing of Tead1 or Tead4 impaired differentiation showing a differential requirement for these factors in PMs and C2C12 cells that involved both differential regulation of their expression and intracellular localisation. Through integration of Tead1 and Tead4 ChIP-seq with chromatin modifications, we identify active enhancers associated with genes activated during C2C12 cell differentiation that are bound by combinations of Tead4, Myod1 or Myog and show a signature of frequently co-occuring motifs. We show that distinct but overlapping sets of genes are deregulated by Tead silencing in C2C12 cells and PMs therefore describing for the first time in a comprehensive manner the specific and redundant regulatory roles of Tead factors in myogenic differentiation. We also performed ChIP-seq from mouse muscle in vivo identifying a set of highly transcribed muscle cell-identity genes and revealing that Tead4 binds a distinct repertoire of sites in C2C12 cells and muscle.
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