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The land plant-specific MIXTA-MYB lineage is implicated in the early evolution of the plant cuticle and the colonization of land

ABSTRACT: We studied gene expression changes in MIXTA-MYB overexpression and knock-out lines compared to the wild type.

ORGANISM(S): Marchantia polymorpha

PROVIDER: GSE155419 | GEO | 2021/12/31

REPOSITORIES: GEO

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The land plant-specific MIXTA-MYB lineage is implicated in the early evolution of the plant cuticle and the colonization of land

Project description:The land plant-specific MIXTA-MYB lineage is implicated in the early evolution of the plant cuticle and the colonization of land

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RNA-seq analysis after MYB (L)/(S) overexpression in Jurkat cells with dTAG-mediated MYB depletion.

Project description:RNA-seq analysis was performed in a T-ALL cell line (Jurkat) with FKBP tag knock-in at the MYB locus to analyze gene expression changes after MYB (L)/(S) overexpression in dTAG-mediated MYB-depleted cells.

2024-11-10 | GSE267372 | GEO

CUT&RUN analysis for phospho-MYB and active histone marks in FKBP-MYB Jurkat cells.

Project description:CUT&RUN analysis was performed in Jurkat cells with FKBP knock-in at the MYB locus to analyze DNA bindings of phospho-MYB, H3K27ac, H3K4me3 after dTAG-mediated depletion.

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MYB-regulated pancreatic cancer secretome

Project description:Earlier we have shown important roles of MYB in pancreatic tumor pathobiology. To better understand the role of MYB in the tumor microenvironment and identify MYB-associated secreted biomarker proteins, we conducted mass spectrometry analysis of the secretome from MYB-modulated and control pancreatic cancer cell lines. We also performed in silico analyses to determine MYB-associated biofunctions, gene networks and altered biological pathways. We further investigated the secreted proteins for their potential biomarker properties.

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MAZ induces MYB expression during the exit from quiescence via the E2F site in the MYB promoter

Project description:Most E2F-binding sites repress transcription through the recruitment of Retinoblasoma (RB) family members until the end of the G1 cell-cycle phase. Although the MYB promoter contains an E2F-binding site, its transcription is activated shortly after the exit from quiescence, before RB family members inactivation, by unknown mechanisms. We had previously uncovered a nuclear factor distinct from E2F, Myb-sp, whose DNA-binding site overlapped the E2F element and had hypothesized that this factor might overcome the transcriptional repression of MYB by E2F-RB family members. We have purified Myb-sp and discovered that Myc-associated zinc finger proteins (MAZ) are major components. We show that various MAZ isoforms are present in Myb-sp and activate transcription via the MYB-E2F element. Moreover, while forced RB or p130 expression repressed the activity of a luciferase reporter driven by the MYB-E2F element, co-expression of MAZ proteins not only reverted repression, but also activated transcription. Finally, we show that MAZ binds the MYB promoter in vivo, that its binding site is critical for MYB transactivation, and that MAZ knockdown inhibits MYB expression during the exit from quiescence. Together, these data indicate that MAZ is essential to bypass MYB promoter repression by RB family members and to induce MYB expression.

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Transcriptome sequencing of K562 cells stably expressing SUMO negative MYB

Project description:We expanded our previously reported transcriptome profiling of K-562 cells (GSE85187) by analyzing the global transcriptional change upon rescue of endogenous MYB knock down (KD) with SUMO-conjugation deficient mutant of MYB (2KR-MYB) and SUMO-binding deficient mutant of MYB (ANAA-MYB) in comparison with K-562 cells treated with siGENOME non-targeting siRNA (GSE85187) , endogenous MYB KD treated with si2992 (GSE85187), rescue of endogenous MYB KD with wild-type MYB (GSE85187) and rescue of endogenous MYB KD with D152V mutant of MYB (GSE85187).

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RNA-seq analysis after dTAG-mediated MYB depletion in Jurkat cells

Project description:RNA-seq analysis was performed in a T-ALL cell line (Jurkat) with FKBP tag knock-in at the MYB locus to analyze gene expression changes after dTAG-mediated MYB depletion.

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A phenol-enriched cuticle is ancestral to lignin evolution in land plants.

Project description:Lignin, one of the most abundant biopolymers on Earth, derives from the plant phenolic metabolism. It appeared upon terrestrialization and is thought critical for plant colonization of land. Early diverging land plants do not form lignin, but already have elements of its biosynthetic machinery. Here we delete in a moss the P450 oxygenase that defines the entry point in angiosperm lignin metabolism, and find that its pre-lignin pathway is essential for development. This pathway does not involve biochemical regulation via shikimate coupling, but instead is coupled with ascorbate catabolism, and controls the synthesis of the moss cuticle, which prevents desiccation and organ fusion. These cuticles share common features with lignin, cutin and suberin, and may represent the extant representative of a common ancestor. Our results demonstrate a critical role for the ancestral phenolic metabolism in moss erect growth and cuticle permeability, consistent with importance in plant adaptation to terrestrial conditions.

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