scholarly journals BRI1 controls vascular cell fate in the Arabidopsis root through RLP44 and phytosulfokine signaling

2018 ◽  
Vol 115 (46) ◽  
pp. 11838-11843 ◽  
Author(s):  
Eleonore Holzwart ◽  
Apolonio Ignacio Huerta ◽  
Nina Glöckner ◽  
Borja Garnelo Gómez ◽  
Friederike Wanke ◽  
...  
Keyword(s):  
Cell Fate ◽  
Stem Cell Niche ◽  
Peptide Hormone ◽  
Vascular Cell ◽  
Arabidopsis Root ◽  
Extrinsic Cues ◽  
Brassinosteroid Signaling ◽  
Procambial Cell ◽  
Cell Niche ◽  
And Function

Multicellularity arose independently in plants and animals, but invariably requires a robust determination and maintenance of cell fate that is adaptive to the environment. This is exemplified by the highly specialized water- and nutrient-conducting cells of the plant vasculature, the organization of which is already prepatterned close to the stem-cell niche, but can be modified according to extrinsic cues. Here, we show that the hormone receptor BRASSINOSTEROID INSENSITIVE 1 (BRI1) is required for root vascular cell-fate maintenance, as BRI1 mutants show ectopic xylem in procambial position. However, this phenotype seems unrelated to canonical brassinosteroid signaling outputs. Instead, BRI1 is required for the expression and function of its interacting partner RECEPTOR-LIKE PROTEIN 44 (RLP44), which, in turn, associates with the receptor for the peptide hormone phytosulfokine (PSK). We show that PSK signaling is required for the maintenance of procambial cell identity and quantitatively controlled by RLP44, which promotes complex formation between the PSK receptor and its coreceptor. Mimicking the loss of RLP44, PSK-related mutants show ectopic xylem in the position of the procambium, whereas rlp44 is rescued by exogenous PSK. Based on these findings, we propose that RLP44 controls cell fate by connecting BRI1 and PSK signaling, providing a mechanistic framework for the dynamic balancing of signaling mediated by the plethora of plant receptor-like kinases at the plasma membrane.

scholarly journals Integration of Brassinosteroid and Phytosulfokine Signalling Controls Vascular Cell Fate in the Arabidopsis Root

2018 ◽  
Author(s):  
Eleonore Holzwart ◽  
Apolonio Ignacio Huerta ◽  
Nina Glöckner ◽  
Borja Garnelo Gómez ◽  
Friederike Ladwig ◽  
...  
Keyword(s):  
Plasma Membrane ◽  
Complex Formation ◽  
Cell Fate ◽  
Hormone Receptor ◽  
Terminal Differentiation ◽  
Peptide Hormone ◽  
Vascular Cell ◽  
Arabidopsis Root ◽  
Procambial Cell ◽  
And Function

AbstractMulticellularity arose independently in plants and animals, but invariably requires robust determination and maintenance of cell fate. This is exemplified by the highly specialized water-and nutrient-conducting cells of the plant vasculature, which are specified long before their commitment to terminal differentiation. Here, we show that the hormone receptor BRASSINOSTEROID INSENSITIVE 1 (BRI1) is required for root vascular cell fate maintenance, as BRI1 mutants show ectopic xylem in procambial position. However, this phenotype is unrelated to classical brassinosteroid signalling outputs. Instead, BRI1 is required for the expression and function of its interaction partner RECEPTOR-LIKE PROTEIN 44 (RLP44), which, in turn, associates with the receptor for the peptide hormone phytosulfokine (PSK). We show that PSK signalling is required for the maintenance of procambial cell identity and is quantitatively controlled by RLP44, which promotes complex formation between the receptor for PSK and its co-receptor. Mimicking the loss of RLP44, PSK-related mutants show ectopic xylem in the position of procambium, whereas rlp44 can be rescued by exogenous PSK. Based on these findings, we propose that RLP44 controls cell fate by connecting BRI1 and PSK signalling, providing a mechanistic framework for the integration of signalling mediated by the plethora of plant receptor-like kinases at the plasma membrane.

scholarly journals Cancer Stem Cells: Repair Gone Awry?

2011 ◽  
Vol 2011 ◽  
pp. 1-11 ◽  
Author(s):  
Fatima Rangwala ◽  
Alessia Omenetti ◽  
Anna Mae Diehl
Keyword(s):  
Cell Fate ◽  
Stem Cell Niche ◽  
Progenitor Cell ◽  
Tissue Injury ◽  
Structure And Function ◽  
Cell Turnover ◽  
Normal Organ ◽  
Liver Cancers ◽  
Cell Niche ◽  
And Function

Because cell turnover occurs in all adult organs, stem/progenitor cells within the stem-cell niche of each tissue must be appropriately mobilized and differentiated to maintain normal organ structure and function. Tissue injury increases the demands on this process, and thus may unmask defective regulation of pathways, such as Hedgehog (Hh), that modulate progenitor cell fate. Hh pathway dysregulation has been demonstrated in many types of cancer, including pancreatic and liver cancers, in which defective Hh signaling has been linked to outgrowth of Hh-responsive cancer stem-initiating cells and stromal elements. Hence, the Hh pathway might be a therapeutic target in such tumors.

scholarly journals Hormonal Regulation of Stem Cell Proliferation at the Arabidopsis thaliana Root Stem Cell Niche

2021 ◽  
Vol 12 ◽  
Author(s):  
Mónica L. García-Gómez ◽  
Adriana Garay-Arroyo ◽  
Berenice García-Ponce ◽  
María de la Paz Sánchez ◽  
Elena R. Álvarez-Buylla
Keyword(s):  
Cell Proliferation ◽  
Arabidopsis Thaliana ◽  
Stem Cell ◽  
Cell Fate ◽  
Regulatory Network ◽  
Hormonal Regulation ◽  
Stem Cell Niche ◽  
Quiescent Center ◽  
Root Stem Cell ◽  
Cell Niche

The root stem cell niche (SCN) of Arabidopsis thaliana consists of the quiescent center (QC) cells and the surrounding initial stem cells that produce progeny to replenish all the tissues of the root. The QC cells divide rather slowly relative to the initials, yet most root tissues can be formed from these cells, depending on the requirements of the plant. Hormones are fundamental cues that link such needs with the cell proliferation and differentiation dynamics at the root SCN. Nonetheless, the crosstalk between hormone signaling and the mechanisms that regulate developmental adjustments is still not fully understood. Developmental transcriptional regulatory networks modulate hormone biosynthesis, metabolism, and signaling, and conversely, hormonal responses can affect the expression of transcription factors involved in the spatiotemporal patterning at the root SCN. Hence, a complex genetic–hormonal regulatory network underlies root patterning, growth, and plasticity in response to changing environmental conditions. In this review, we summarize the scientific literature regarding the role of hormones in the regulation of QC cell proliferation and discuss how hormonal signaling pathways may be integrated with the gene regulatory network that underlies cell fate in the root SCN. The conceptual framework we present aims to contribute to the understanding of the mechanisms by which hormonal pathways act as integrators of environmental cues to impact on SCN activity.

scholarly journals ULTRAPETALA1 maintains Arabidopsis root stem cell niche independently of ARABIDOPSIS TRITHORAX1

2019 ◽  
Vol 225 (3) ◽  
pp. 1261-1272
Author(s):  
Diego Ornelas‐Ayala ◽  
Rosario Vega‐León ◽  
Emilio Petrone‐Mendoza ◽  
Adriana Garay‐Arroyo ◽  
Berenice García‐Ponce ◽  
...  
Keyword(s):  
Stem Cell ◽  
Stem Cell Niche ◽  
Arabidopsis Root ◽  
Root Stem Cell ◽  
Cell Niche

scholarly journals The galactocerebrosidase enzyme contributes to the maintenance of a functional hematopoietic stem cell niche

Blood ◽  
2010 ◽  
Vol 116 (11) ◽  
pp. 1857-1866 ◽  
Author(s):  
Ilaria Visigalli ◽  
Silvia Ungari ◽  
Sabata Martino ◽  
Hyejung Park ◽  
Martina Cesani ◽  
...  
Keyword(s):  
Stem Cell ◽  
Stem Cell Niche ◽  
Disease Model ◽  
Cell Types ◽  
Hematopoietic Stem ◽  
Hematopoietic Stem Cell Niche ◽  
Intracellular Content ◽  
Cell Niche ◽  
And Function ◽  
Globoid Cell

Abstract The balance between survival and death in many cell types is regulated by small changes in the intracellular content of bioactive sphingolipids. Enzymes that either produce or degrade these sphingolipids control this equilibrium. The findings here described indicate that the lysosomal galactocerebrosidase (GALC) enzyme, defective in globoid cell leukodystrophy, is involved in the maintenance of a functional hematopoietic stem/progenitor cell (HSPC) niche by contributing to the control of the intracellular content of key sphingolipids. Indeed, we show that both insufficient and supraphysiologic GALC activity—by inherited genetic deficiency or forced gene expression in patients' cells and in the disease model—induce alterations of the intracellular content of the bioactive GALC downstream products ceramide and sphingosine, and thus affect HSPC survival and function and the functionality of the stem cell niche. Therefore, GALC and, possibly, other enzymes for the maintenance of niche functionality and health tightly control the concentration of these sphingolipids within HSPCs.

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