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Expression data from dark grown Arabidopsis Wild type (Wt, col-o) and pif1-2 (At2g20810, Salk_072677) mutant seedlings

ABSTRACT: Arabidopsis bHLH transcription factor PIF1 has been shown function as a negative regulator of Chlorophyll biosynthesis. Pif1-2 mutant accumulate more protochlorophylide during prolonged dark growth condations, therefore the comparation between Wt and pif1-2 mutant will help us find the PIF1 target genes in Chlorophyll biosynthesis pathway at genome wide level under the dark grown conditions. We used microarrays to detail the global gene expression under the regulation of PIF1. Keywords: Genotype comparison

ORGANISM(S): Arabidopsis thaliana

PROVIDER: GSE11594 | GEO | 2008/05/30

SECONDARY ACCESSION(S): PRJNA106231

REPOSITORIES: GEO

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Transcription profiling by array of Arabidopsis seedlings mutant for pif1

Project description:Arabidopsis bHLH transcription factor PIF1 has been shown function as a negative regulator of Chlorophyll biosynthesis. Pif1-2 mutant accumulate more protochlorophylide during prolonged dark growth condations, therefore the comparation between Wt and pif1-2 mutant will help us find the PIF1 target genes in Chlorophyll biosynthesis pathway at genome wide level under the dark grown conditions. We used microarrays to detail the global gene expression under the regulation of PIF1. Experiment Overall Design: 4 days dark grown Wt and pif1-2 seedlings were collected for isolation RNA. Standard Affymetrix protocal and 25K Affymetrix chip (ATH1) were used for Microarry hybridition.

2008-06-18 | E-GEOD-11594 | biostudies-arrayexpress

Expression changes by Endodermal PIF1: SCR:PIF1/pifQ transgenic plant vs. pif1pif3pif4pif5 (pifQ) mutant

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Expression changes by Endodermal PIF1: SCR:PIF1/pifQ transgenic plant vs. pif1pif3pif4pif5 (pifQ) mutant

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2009-10-27 | E-GEOD-18631 | biostudies-arrayexpress

Genome-wide identification of PIF1-binding sites and direct-target genes of PIF1 transcriptional regulation in skotomorphogenesis

Project description:Dark-grown seedlings exhibit skotomorphogenic development. Genetic and molecular evidence indicates that a quartet of Arabidopsis Phytochrome (phy)-Interacting bHLH Factors (PIF1, 3, 4 and 5) are critically necessary to maintaining this developmental state, and that light activation of phy induces a switch to photomorphogenic development by inducing rapid degradation of the PIFs. Here, using combined ChIP-seq and RNA-seq analyses, we have identified genes that are direct targets of PIF1 transcriptional regulation, and we provide evidence that the quartet collectively regulate these genes by shared, direct binding to the target promoters in promoting skotomorphogenesis.

2014-10-02 | GSE43283 | GEO

Genome-wide identification of PIF1-binding sites and direct-target genes of PIF1 transcriptional regulation in skotomorphogenesis

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Expression from dark grown Arabidopsis Wild type (Wt, Col-o) and ein3-1eil1-1 (AT3G20770, AT2G27050) mutant seedlings

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Arabidopsis dark-induced senescence: wild type (Col-0) vs. pif quadruple (pif1pif3pif4pif5) mutant

Project description:Transcriptional profiling of Arabidopsis dark-induced senescence comparing wild type (Col-0) with pif quadruple (pif1/3/4/5) mutant. After synchronized germination, the plants were grown under continuous white light for 7 days and transferred to darkness for 2 days to induce senescence. Goal was to determine the effect of PIFs on transcriptomic regulation during dark-induced senescence.

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Gene expression in pif1pif3pif4pif5 mutant under dark or red light conditions

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Lack of the pif1 helicase enhances zinc tolerance in S. cerevisiae

Project description:The Saccharomyces cerevisiae gene PIF1 encodes a conserved eukaryotic DNA helicase required for both mitochondrial and nuclear DNA integrity. Our previous work revealed that a pif1D strain is tolerant to zinc overload. We demonstrate here that this effect is independent of the Pif1 helicase activity and is only observed when the protein is absent from the mitochondria. pif1 cells accumulate abnormal amounts of mitochondrial zinc and iron. Transcriptional profiling reveals that pif1 cells under standard growth conditions overexpress aconitase-related genes. When exposed to zinc, pif1 cells show lower induction of genes encoding iron (siderophores) transporters and higher expression of genes related to oxidative stress responses than wild type cells. Coincidently, pif1 mutants are less prone to zinc-induced oxidative stress and display a higher reduced/oxidized glutathione ratio. Strikingly, although pif1 cells contain normal amounts of the Aco1 protein, they completely lack aconitase activity. Loss of Aco1 activity is also observed when the cell expresses a non-mitochondrially targeted form of Pif1. We postulate that lack of Pif1 forces aconitase to play its DNA protective role as nucleoid protein and that this would trigger a domino effect on iron homeostasis resulting in increased zinc tolerance. Four samples were analyzed: WT and pif1 mutant both, in the presence and in the absence of 5 mM ZnCl2 for 1 h. We compared the expression profile of: 1) WT+Zn vs WT-Zn, 2) pif1 mutant+Zn vs pif1 mutant-Zn, 3) pif1 mutant vs WT, and 4) pif1 mutant+Zn vs WT+Zn. A Dye-swap was carried out for each comparison of samples. Total number of chips analyzed: 8.

2010-05-31 | E-GEOD-18411 | biostudies-arrayexpress

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