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Cell layer specific and polysome associated RNA from Arabidopsis thaliana Col0 and hyl1 mutant roots.

ABSTRACT: Cell layer specific and polysome associated RNA from Arabidopsis thaliana Col0 and hyl1 mutant roots.

PROVIDER: PRJNA408295 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR6057930_1.fastq.gz	Fastqsanger.gz
	SRR6057930_2.fastq.gz	Fastqsanger.gz
	SRR6057940_1.fastq.gz	Fastqsanger.gz
	SRR6057940_2.fastq.gz	Fastqsanger.gz
	SRR6057931_1.fastq.gz	Fastqsanger.gz

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Cell layer specific AGO1-loaded sRNA from dcl234 triple mutant Cell layer specific and polysome associated RNA from Col0 and hyl1 mutant roots.

Project description:Cell layer specific AGO1-loaded sRNA from dcl234 triple mutant Cell layer specific and polysome associated RNA from Col0 and hyl1 mutant roots.

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Cell layer specific and polysome associated RNA from Arabidopsis thaliana Col0 and hyl1 mutant roots.

Project description:microRNAs (miRNA’s) regulation target gene expression, often transcription factors and as such control entire transcriptional networks. This control is important for various developmental transitions and stress responses in a wide range of eukaryotic organisms. While miRNA-mediated gene regulation has been investigated over time (temporal) and in whole organs or tissues in multiple different organisms highlighting their importance, there has been a distinct lack of focus on spatial resolution of miRNA biology. Here we present at cell-type specific resolution, miRNA loading and miRNA action within the Arabidopsis root. Our results for the first time demonstrate the multiple novel modes of miRNA action and illustrate the widespread nature of miRNA movement, at a genome scale within a complex eukaryotic organ.

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Cell layer specific AGO1-loaded sRNA from dcl234 triple mutant; Cell layer specific and polysome associated RNA from Col0 and hyl1 mutant roots.

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Project description:DCL1 and HYL1 are the core components of miRNA biogenesis machinery. hyl1-null mutants accumulate low levels of miRNAs and cause pleiotropic morphological phenotypes. Here, we reported that we identified 5 new alleles of DCL1 which are able to suppress the hyl1 morphological phenotypes and restore the miRNA accumulation level in hyl1 plants. These new alleles are located in the helicase and RNaseIIIa domains of DCL1, highlighting the critical functions of these domains. Biochemical analyses of these suppressors indicated that they process pri-miRNA more efficiently, with both higher Kcat and lower Km values. In addition, we investigated the functions of the DCL1 helicase domain. Our results indicated that the helicase domain is able to modulate the DCL1 processing activities. Based on these results, we proposed that HYL1 might exert its function through interaction with the DCL1 helicase domain. Small RNA sequencing from hyl1 and select hyl1/dcl1 suppressor mutants confirms thats suppression of the hyl1 phenotype is due to an increase in the accumulation, but not the precision, of miRNAs in the suppressor mutants. Wild-type, hyl1-2, hyl1-2/dcl1-20, and hyl1-2/dcl1-21 plants were sampled from both rosette leaves and flowers.

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