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Redundancies in low K signaling of neo-tetraploids leads in increased shoot K

ABSTRACT: Redundancies in low K signaling of neo-tetraploids leads in increased shoot K

PROVIDER: PRJNA749718 | ENA |

REPOSITORIES: ENA

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Redundancies in low K signaling of neo-tetraploids leads in increased shoot K [RNA-seq_1]

Project description:Whole Genome Duplication (WGD) events occurred frequently during land plant evolution and their long term benefits to neo-functionalization of genes and speciation is well known (Baduel et al., 2018). However short term benefits, important for the establishment of a new population, are more difficult to observe until Chao et al., 2013 described a fitness advantage under high salinity. Additionally shoot K levels were higher in neo-tetraploids, an important feature since K uptake becomes increasingly more difficult on highly saline soil. The molecular basis for these phenotypes was not known. Here we analyze neo-tetraploid Arabidopsis thaliana plants using RNAseq and ICP-MS to evaluate the effect of mutations and ploidy on the gene expression and shoot ionome. We are able to show that neo-tetraploid plants induce low-potassium (K) signaling to increase their shoot K content. However, we also show that this low-K signaling is distinct form previously studied, externally applied low-K signaling. In this way, we are able to identify new components of the K homeostasis network, which are required to regulate K demand. Additionally we are able to show that while individual components of the K uptake system are not sufficient to increase shoot K, a loss of root hairs abolished the ploidy K phenotype (PPP) as does a defective Casparian strip. Root hairs are the site of entry of K into the root and neo-tetraploids increase their root hair length and density (RHI) to facilitate their higher K demand. The Casparian strip on the other hand enables higher K concentration in the stele of the root, which is required for the increased K content in neo-tetraploids.

2022-07-31 | GSE180004 | GEO

Redundancies in low K signaling of neo-tetraploids leads in increased shoot K [RNA-seq_2]

2022-07-31 | GSE180818 | GEO

Redundancies in low K signaling of neo-tetraploids leads in increased shoot K [RNA-seq_2]

Project description:Redundancies in low K signaling of neo-tetraploids leads in increased shoot K [RNA-seq_2]

| PRJNA749717 | ENA

Redundancies in low K signaling of neo-tetraploids leads in increased shoot K [RNA-seq_1]

Project description:Redundancies in low K signaling of neo-tetraploids leads in increased shoot K [RNA-seq_1]

| PRJNA746250 | ENA

Redundancies in low K signaling of neo-tetraploids leads in increased shoot K

Project description:This SuperSeries is composed of the SubSeries listed below.

2022-07-31 | GSE180819 | GEO

Alteration of TAC1 expression in Prunus species leads to pleiotropic shoot phenotypes

Project description:Alteration of TAC1 expression in Prunus species leads to pleiotropic shoot phenotypes

| PRJNA448600 | ENA

Hypoxia Mediated Downregulation of miRNA Biogenesis Leads to Increased Tumor Progression

Project description:Hypoxia Mediated Downregulation of miRNA Biogenesis Leads to Increased Tumor Progression

| PRJNA229957 | ENA

HCaRG vs NEO

Project description:Summary: HEK293 cells were transfected with control plasmid (pcDNA1/Neo; Invitrogen) or with the plasmid encoding HCaRG by a standard calcium phosphate co-precipitation method. The clones expressing the highest levels of HCaRG, HCaRG clone 8 and 9 were used in this experiment, while clone transfected with vector alone, Neo clone, served as control. Stable transfectants were synchronized and grown in the presence of 10% FBS for 48 h. Total RNAs were purified with the mini RNeasy kit (Qiagen). Keywords: parallel sample

2006-10-27 | GSE4737 | GEO

RET overexpression leads to increased brain metastatic competency in luminal breast cancer

Project description:RET overexpression leads to increased brain metastatic competency in luminal breast cancer

| PRJNA987983 | ENA

Tet2 loss leads to increased hematopoietic stem cell self-renewal and myeloid transformation

Project description:Recurrent somatic mutations in TET2 and in other genes that regulate the epigenetic state have been identified in patients with myeloid malignancies and in other cancers. However, the in vivo effects of Tet2 loss have not been delineated. We report here that Tet2 loss leads to increased stem-cell self-renewal and to progressive stem cell expansion. Consistent with human mutational data, Tet2 loss leads to myeloproliferation in vivo, notable for splenomegaly and monocytic proliferation. In addition, haploinsufficiency for Tet2 confers increased self-renewal and myeloproliferation, suggesting that the monoallelic TET2 mutations found in most TET2-mutant leukemia patients contribute to myeloid transformation. This work demonstrates that absent or reduced Tet2 function leads to enhanced stem cell function in vivo and to myeloid transformation. These studies show that a ubiquitin ligase-substrate pair can orchestrate the molecular program of HSC differentitiation Gene expression profiles from WT and Tet2-/- sorted LSK and myeloid progenitors (CMP and GMP) were compared using genome wide mRNA expression profiling by Affymetrix genechip arrays (Mouse 430 2.0) and key targets were validated by chromatin immunoprecipitation experiments.

2011-07-01 | E-GEOD-27816 | biostudies-arrayexpress

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