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Bird Factors integrate positional signals to coordinate asymmetric cell division and cell fate

ABSTRACT: We sorted for GFP+ cells using the enhancer trap J0571 with the UAS promoter driving the expression of different BIRD genes. Different genetic backgrounds are use and listed below. Seedlings were grown for 5 days. J0571 and J0571-UAS-BIRDS sorted fluorecent cells were harvested for RNA extraction.

ORGANISM(S): Arabidopsis thaliana

SUBMITTER: Rosangela Sozzani

PROVIDER: E-GEOD-60157 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Transcriptional control of tissue formation throughout root development.

Moreno-Risueno Miguel A MA Sozzani Rosangela R Yardımcı Galip Gürkan GG Petricka Jalean J JJ Vernoux Teva T Blilou Ikram I Alonso Jose J Winter Cara M CM Ohler Uwe U Scheres Ben B Benfey Philip N PN

Science (New York, N.Y.) 20151001 6259

Tissue patterns are dynamically maintained. Continuous formation of plant tissues during postembryonic growth requires asymmetric divisions and the specification of cell lineages. We show that the BIRDs and SCARECROW regulate lineage identity, positional signals, patterning, and formative divisions throughout Arabidopsis root growth. These transcription factors are postembryonic determinants of the ground tissue stem cells and their lineage. Upon further activation by the positional signal SHORT ...[more]

PMID: 26494755

Similar Datasets

Bird Factors integrate positional signals to coordinate asymmetric cell division and cell fate

Project description:We sorted for GFP+ cells using the enhancer trap J0571 with the UAS promoter driving the expression of different BIRD genes. Different genetic backgrounds are use and listed below.

2015-11-02 | GSE60157 | GEO

The SHR/SCR pathway directly activates genes involved in asymmetric cell division in the Arabidopsis root

Project description:Asymmetric division of cortex/endodermal initials (CEI) in the Arabidopsis root generates two layers of ground tissue and is controlled by a finely orchestrated interplay between the transcription factors, SHORT ROOT (SHR) and SCARECROW (SCR). To understand the dynamics of the SHR/SCR regulatory network we performed microarray time course experiments using inducible versions of SHR and SCR and examined their transcriptional effects specifically in the ground tissue. Keywords: SHR and SCR time course and CEI cell-type analyses We performed a time course analysis (TC data set) of the ground tissue (sorted J0571 enancher trap) after transfer either SHR or SCR inducible plants to Dex containing plates 0, 1, 3, 6 and 12 hours. We sorted for CEI cells using the pCYCD6::GFP marker line. Seedlings were grown for 5 days. SHR and SCR inducible plants were transfer to 1microM Dex MS plates. J0571 and CYCD6 sorted fluorecent cells were harvested for RNA extraction.

2010-07-19 | E-GEOD-15876 | biostudies-arrayexpress

PAR-4 and anillin regulate myosin to coordinate spindle and furrow position during asymmetric division.

Project description:During asymmetric cell division, the mitotic spindle and polarized myosin can both determine the position of the cytokinetic furrow. However, how cells coordinate signals from the spindle and myosin to ensure that cleavage occurs through the spindle midzone is unknown. Here, we identify a novel pathway that is essential to inhibit myosin and coordinate furrow and spindle positions during asymmetric division. In Caenorhabditis elegans one-cell embryos, myosin localizes at the anterior cortex whereas the mitotic spindle localizes toward the posterior. We find that PAR-4/LKB1 impinges on myosin via two pathways, an anillin-dependent pathway that also responds to the cullin CUL-5 and an anillin-independent pathway involving the kinase PIG-1/MELK. In the absence of both PIG-1/MELK and the anillin ANI-1, myosin accumulates at the anterior cortex and induces a strong displacement of the furrow toward the anterior, which can lead to DNA segregation defects. Regulation of asymmetrically localized myosin is thus critical to ensure that furrow and spindle midzone positions coincide throughout cytokinesis.

| S-EPMC4586735 | biostudies-literature

Targets of ALTERED PHLOEM DEVELOPMENT (APL)

Project description:We profiled transcripts from sorted phloem cells of wild-type and apl mutants to identify the genes regulated by APL in phloem. We profiled transcripts from sorted phloem cells of wild-type and apl mutants to identify the genes regulated by APL in phloem. Three biological replicates for control WT and apl mutants were used in thes study. Root tissue was protoplasted and sorted using fluorescence-activated cell sorting (FACS). Total RNA was extracted from GFP+ protoplasts.

2014-08-25 | E-GEOD-55222 | biostudies-arrayexpress

Restriction on self-renewing asymmetric division is coupled to terminal asymmetric division in the Drosophila CNS.

Project description:Neuronal precursor cells undergo self-renewing and non-self-renewing asymmetric divisions to generate a large number of neurons of distinct identities. In Drosophila, primary precursor neuroblasts undergo a varying number of self-renewing asymmetric divisions, with one known exception, the MP2 lineage, which undergoes just one terminal asymmetric division similar to the secondary precursor cells. The mechanism and the genes that regulate the transition from self-renewing to non-self-renewing asymmetric division or the number of times a precursor divides is unknown. Here, we show that the T-box transcription factor, Midline (Mid), couples these events. We find that in mid loss of function mutants, MP2 undergoes additional self-renewing asymmetric divisions, the identity of progeny neurons generated dependent upon Numb localization in the parent MP2. MP2 expresses Mid transiently and an over-expression of mid in MP2 can block its division. The mechanism which directs the self-renewing asymmetric division of MP2 in mid involves an upregulation of Cyclin E. Our results indicate that Mid inhibits cyclin E gene expression by binding to a variant Mid-binding site in the cyclin E promoter and represses its expression without entirely abolishing it. Consistent with this, over-expression of cyclin E in MP2 causes its multiple self-renewing asymmetric division. These results reveal a Mid-regulated pathway that restricts the self-renewing asymmetric division potential of cells via inhibiting cyclin E and facilitating their exit from cell cycle.

| S-EPMC7521697 | biostudies-literature

The WT1-like transcription factor Klumpfuss maintains lineage commitment in the intestine

Project description:RNA-Seq experiment of sorted Esg+ stem-progenitors expressing either RNA (kluRNAi) against Klu or overexpression of klu (UAS-klu)

2019-07-26 | GSE132243 | GEO

Asymmetric cancer cell division regulated by AKT.

Project description:Human tumors often contain slowly proliferating cancer cells that resist treatment, but we do not know precisely how these cells arise. We show that rapidly proliferating cancer cells can divide asymmetrically to produce slowly proliferating "G0-like" progeny that are enriched following chemotherapy in breast cancer patients. Asymmetric cancer cell division results from asymmetric suppression of AKT/PKB kinase signaling in one daughter cell during telophase of mitosis. Moreover, inhibition of AKT signaling with small-molecule drugs can induce asymmetric cancer cell division and the production of slow proliferators. Cancer cells therefore appear to continuously flux between symmetric and asymmetric division depending on the precise state of their AKT signaling network. This model may have significant implications for understanding how tumors grow, evade treatment, and recur.

| S-EPMC3150943 | biostudies-literature

Control of apoptosis by asymmetric cell division.

Project description:Asymmetric cell division and apoptosis (programmed cell death) are two fundamental processes that are important for the development and function of multicellular organisms. We have found that the processes of asymmetric cell division and apoptosis can be functionally linked. Specifically, we show that asymmetric cell division in the nematode Caenorhabditis elegans is mediated by a pathway involving three genes, dnj-11 MIDA1, ces-2 HLF, and ces-1 Snail, that directly control the enzymatic machinery responsible for apoptosis. Interestingly, the MIDA1-like protein GlsA of the alga Volvox carteri, as well as the Snail-related proteins Snail, Escargot, and Worniu of Drosophila melanogaster, have previously been implicated in asymmetric cell division. Therefore, C. elegans dnj-11 MIDA1, ces-2 HLF, and ces-1 Snail may be components of a pathway involved in asymmetric cell division that is conserved throughout the plant and animal kingdoms. Furthermore, based on our results, we propose that this pathway directly controls the apoptotic fate in C. elegans, and possibly other animals as well.

| S-EPMC2288629 | biostudies-literature

BASL controls asymmetric cell division in Arabidopsis.

Project description:Development in multicellular organisms requires the organized generation of differences. A universal mechanism for creating such differences is asymmetric cell division. In plants, as in animals, asymmetric divisions are correlated with the production of cellular diversity and pattern; however, structural constraints imposed by plant cell walls and the absence of homologs of known animal or fungal cell polarity regulators necessitates that plants utilize new molecules and mechanisms to create asymmetries. Here, we identify BASL, a novel regulator of asymmetric divisions in Arabidopsis. In asymmetrically dividing stomatal-lineage cells, BASL accumulates in a polarized crescent at the cell periphery before division, and then localizes differentially to the nucleus and a peripheral crescent in self-renewing cells and their sisters after division. BASL presence at the cell periphery is critical for its function, and we propose that BASL represents a plant-specific solution to the challenge of asymmetric cell division.

| S-EPMC4105981 | biostudies-literature

Transcriptional profiling of esg+-midgut progenitor cells expressing esgRNAi or UAS-esg AND of whole midgut tissue from flies overexpressing UAS-esg in enterocyte (EC) cells

Project description:RNA-Seq of amplified mRNA from sorted esg+-midgut progenitor cells expressing esgRNAi or UAS-esg AND RNA-Seq of whole midgut tissue from flies overexpressing UAS-esg and UAS-esg+UAS-dIAP (+control empty vector RNAi, UAS-dIAP and w1118) using the MyoIA-Gal4ts EC-driver

2014-10-25 | E-MTAB-2915 | biostudies-arrayexpress

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