scholarly journals Control of Arabidopsis shoot stem cell homeostasis by two antagonistic CLE peptide signalling pathways

eLife ◽  
2021 ◽  
Vol 10 ◽  
Author(s):  
Jenia Schlegel ◽  
Gregoire Denay ◽  
Rene H Wink ◽  
Karine Gustavo Pinto ◽  
Yvonne Stahl ◽  
...  
Keyword(s):  
Stem Cell ◽  
Cell Differentiation ◽  
Negative Feedback ◽  
Feedback Loop ◽  
Cell Activity ◽  
Negative Feedback Loop ◽  
Dependent Manner ◽  
Gene Encoding ◽  
Cell Homeostasis ◽  
Cle Peptide

Stem cell homeostasis in plant shoot meristems requires tight coordiantion between stem cell proliferation and cell differentiation. In Arabidopsis, stem cells express the secreted dodecapeptide CLAVATA3 (CLV3), which signals through the leucine-rich repeat (LRR)-receptor kinase CLAVATA1 (CLV1) and related CLV1-family members to downregulate expression of the homeodomain transcription factor WUSCHEL (WUS). WUS protein moves from cells below the stem cell domain to the meristem tip and promotes stem cell identity, together with CLV3 expression, generating a negative feedback loop. How stem cell activity in the meristem centre is coordinated with organ initiation and cell differentiation at the periphery is unknown. We show here that the CLE40 gene, encoding a secreted peptide closely related to CLV3, is expressed in the SAM in differentiating cells in a pattern complementary to that of CLV3. CLE40 promotes WUS expression via BAM1, a CLV1-family receptor, and CLE40 expression is in turn repressed in a WUS-dependent manner. Together, CLE40-BAM1-WUS establish a second negative feedback loop. We propose that stem cell homeostasis is achieved through two intertwined pathways that adjust WUS activity and incorporate information on the size of the stem cell domain, via CLV3-CLV1, and on cell differentiation via CLE40-BAM1.

scholarly journals Control of Arabidopsis shoot stem cell homeostasis by two antagonistic CLE peptide signalling pathways

2021 ◽  
Author(s):  
Jenia Schlegel ◽  
Gregoire Denay ◽  
Karine Gustavo Pinto ◽  
Yvonne Stahl ◽  
Julia Schmid ◽  
...  
Keyword(s):  
Stem Cell ◽  
Cell Differentiation ◽  
Negative Feedback ◽  
Feedback Loop ◽  
Cell Activity ◽  
Negative Feedback Loop ◽  
Dependent Manner ◽  
Gene Encoding ◽  
Cell Homeostasis ◽  
Cle Peptide

Stem cell homeostasis in plant shoot meristems requires tight coordination between stem cell proliferation and cell differentiation. In Arabidopsis, stem cells express the secreted dodecapeptide CLAVATA3 (CLV3), which signals through the leucine-rich repeat (LRR)–receptor kinase CLAVATA1 (CLV1) and related CLV1-family members to downregulate expression of the homeodomain transcription factor WUSCHEL (WUS). WUS protein moves from cells below the stem cell domain to the meristem tip and promotes stem cell identity, together with CLV3 expression, generating a negative feedback loop. How stem cell activity in the meristem centre is coordinated with organ initiation and cell differentiation at the periphery is unknown. We show here that the CLE40 gene, encoding a secreted peptide closely related to CLV3, is expressed in the SAM in differentiating cells in a pattern complementary to that of CLV3. CLE40 promotes WUS expression via BAM1, a CLV1-family receptor, and CLE40 expression is in turn repressed in a WUS-dependent manner. Together, CLE40-BAM1-WUS establish a second negative feedback loop. We propose that stem cell homeostasis is achieved through two intertwined pathways that adjust WUS activity and incorporate information on the size of the stem cell domain, via CLV3-CLV1, and on cell differentiation via CLE40-BAM1.

scholarly journals Curcumin inhibits breast cancer stem cell migration by amplifying the E-cadherin/β-catenin negative feedback loop

2014 ◽  
Vol 5 (5) ◽  
pp. 116 ◽  
Author(s):  
Shravanti Mukherjee ◽  
Minakshi Mazumdar ◽  
Samik Chakraborty ◽  
Argha Manna ◽  
Shilpi Saha ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Stem Cell ◽  
Cell Migration ◽  
Cancer Stem Cell ◽  
Negative Feedback ◽  
Feedback Loop ◽  
Breast Cancer Stem Cell ◽  
Negative Feedback Loop ◽  
Stem Cell Migration ◽  
E Cadherin

A negative feedback loop of transcription factors that controls stem cell pluripotency and self‐renewal

2006 ◽  
Vol 20 (10) ◽  
pp. 1730-1732 ◽  
Author(s):  
Guangjin Pan ◽  
Jun Li ◽  
Yali Zhou ◽  
Hui Zheng ◽  
Duanqing Pei ◽  
...  
Keyword(s):  
Stem Cell ◽  
Transcription Factors ◽  
Negative Feedback ◽  
Feedback Loop ◽  
Negative Feedback Loop ◽  
Self Renewal ◽  
Stem Cell Pluripotency

scholarly journals 17-P019 A Pax3/7:Foxc2 negative feedback loop in the somite modulates multipotent stem cell fates

2009 ◽  
Vol 126 ◽  
pp. S276
Author(s):  
Mounia Lagha ◽  
Silvia Brunelli ◽  
Graziella Messina ◽  
Tsutomu Kume ◽  
Frédéric Relaix ◽  
...  
Keyword(s):  
Stem Cell ◽  
Negative Feedback ◽  
Feedback Loop ◽  
Negative Feedback Loop ◽  
Cell Fates ◽  
Multipotent Stem Cell

scholarly journals miR-30a/SOX4 Double Negative Feedback Loop is modulated by Disulfiram and regulates EMT and Stem Cell-like properties in Breast Cancer

2021 ◽  
Vol 12 (16) ◽  
pp. 5053-5065
Author(s):  
Zijian Liu ◽  
Mi Mi ◽  
Xin Zheng ◽  
Caijiao Zhang ◽  
Fang Zhu ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Stem Cell ◽  
Negative Feedback ◽  
Feedback Loop ◽  
Negative Feedback Loop ◽  
Double Negative

scholarly journals A Direct Negative Feedback Loop of miR-4721/FOXA1/Nanog Promotes Nasopharyngeal Cell Stem Cell Enrichment and Metastasis 

2021 ◽  
Author(s):  
Mengyang Zhao ◽  
Zibo Tang ◽  
Yijun Wang ◽  
Jiaojiao Ding ◽  
Ying Guo ◽  
...  
Keyword(s):  
Stem Cells ◽  
Stem Cell ◽  
Negative Feedback ◽  
Feedback Loop ◽  
Side Population ◽  
Nasopharyngeal Cancer ◽  
Luciferase Reporter ◽  
Migration And Invasion ◽  
Negative Feedback Loop ◽  
Linkage Mechanism

Abstract Objective: The recurrence and metastasis of nasopharyngeal cancer (NPC) may be mainly attributed to the persistence of cancer stem cells (CSCs); however, the linkage mechanism has yet to be fully elucidated. Methods: The levels of miR-4721, FOXA1, and Nanog expression in NPC were detected by in situ hybridization and immunohistochemistry. In vivo and in vitro metastasis assays confirmed miR-4721 promotes cell migration and invasion. Tumor spheroid formation assay, side population (SP) assay, and ALDEFLUOR assay verified miR-4721 regulates cancer stem cell-like properties. Luciferase reporter assay showed that miR-4721 directly regulates FOXA1 and FOXA1 effects the promoter activity of miR-4721 and Nanog. Chromatin immunoprecipitation (ChIP) analysis and electrophoresis mobility shift assay (EMSA) revealed that FOXA1 combined the promoter region of human miR-4721 and Nanog and the possible mechanism was also analyzed.Results: In this study, a new mechanism of NPC tumorigenesis related to miR-4721 was verified. We found that miR-4721, FOXA1 and Nanog control their expressions through a negative feedback loop and then activate the downstream regulator of stem cell signaling to promote the enrichment and metastasis of NPC stem cells. Conclusion: These findings elucidate that the feedback loop of miR-4721/FOXA1/Nanog can regulate stemness and metastasis in NPC and may provide an experimental theoretical basis for metastasis and treatment resistance in NPC.

scholarly journals Patterning on the move: the effects of Hh morphogen source movement on signaling dynamics

2021 ◽  
Author(s):  
david G Miguez ◽  
Antonella G Iannini ◽  
diana garcia-morales ◽  
Fernando Casares
Keyword(s):  
Signaling Pathway ◽  
Negative Feedback ◽  
Feedback Loop ◽  
Computational Models ◽  
Compound Eye ◽  
Temporal Dynamics ◽  
Negative Feedback Loop ◽  
Dependent Manner ◽  
Concentration Dependent Manner ◽  
Signaling Dynamics

Morphogens of the Hh-family trigger gene expression changes of receiving cells in a concentration-dependent manner. The outputs of the pathway include regulation of cell identity, proliferation, death or metabolism, depending on the tissue or organ. This variety of responses relies on a conserved signaling pathway. Its internal logic includes a negative feedback loop involving the Hh receptor Ptc. In this paper, we use experiments and computational models to study and compare the different spatial signaling profiles downstream of Hh in several developing Drosophila organs. We show that the spatial distribution of Ptc and the activator form of the Gli transcription factor, CiA, in wing, antenna and ocellus show similar features, but markedly different from that in the compound eye (CE). We show that these two profile types represent two time points along the signaling dynamics, and that the interplay between the spatial displacement of the Hh source in the CE and the negative feedback loop maintains the receiving cells effectively in an earlier stage of signaling. These results indicate that the dynamics of the Hh source strongly influences the signaling profile Hh elicits in receiving cells, and show how the interaction between spatial and temporal dynamics of signaling and differentiation processes can contribute to the informational versatility of the conserved Hh signaling pathway.

scholarly journals A direct negative feedback loop of miR-4721/FOXA1/Nanog promotes nasopharyngeal cell stem cell enrichment and metastasis

2021 ◽  
Vol 19 (1) ◽  
Author(s):  
Mengyang Zhao ◽  
Zibo Tang ◽  
Yijun Wang ◽  
Jiaojiao Ding ◽  
Ying Guo ◽  
...  
Keyword(s):  
Stem Cells ◽  
Stem Cell ◽  
Negative Feedback ◽  
Feedback Loop ◽  
Side Population ◽  
Nasopharyngeal Cancer ◽  
Luciferase Reporter ◽  
Migration And Invasion ◽  
Negative Feedback Loop ◽  
Linkage Mechanism

Abstract Objective The recurrence and metastasis of nasopharyngeal cancer (NPC) may be mainly attributed to the persistence of cancer stem cells (CSCs); however, the linkage mechanism has yet to be fully elucidated. Methods The levels of miR-4721, FOXA1, and Nanog expression in NPC were detected by in situ hybridization and immunohistochemistry. In vivo and in vitro metastasis assays confirmed miR-4721 promotes cell migration and invasion. Tumor spheroid formation assay, side population (SP) assay, and ALDEFLUOR assay verified miR-4721 regulates cancer stem cell-like properties. Luciferase reporter assay showed that miR-4721 directly regulates FOXA1 and FOXA1 effects the promoter activity of miR-4721 and Nanog. Chromatin immunoprecipitation (ChIP) analysis and electrophoresis mobility shift assay (EMSA) revealed that FOXA1 combined the promoter region of human miR-4721 and Nanog and the possible mechanism was also analyzed. Results In this study, a new mechanism of NPC tumorigenesis related to miR-4721 was verified. We found that miR-4721, FOXA1 and Nanog control their expressions through a negative feedback loop and then activate the downstream regulator of stem cell signaling to promote the enrichment and metastasis of NPC stem cells. Conclusion These findings elucidate that the feedback loop of miR-4721/FOXA1/Nanog can regulate stemness and metastasis in NPC and may provide an experimental theoretical basis for metastasis and treatment resistance in NPC.

scholarly journals A novel slug-containing negative-feedback loop regulates SCF/c-Kit-mediated hematopoietic stem cell self-renewal

Leukemia ◽  
2016 ◽  
Vol 31 (2) ◽  
pp. 403-413 ◽  
Author(s):  
Z Zhang ◽  
P Zhu ◽  
Y Zhou ◽  
Y Sheng ◽  
Y Hong ◽  
...  
Keyword(s):  
Stem Cell ◽  
Hematopoietic Stem Cell ◽  
Negative Feedback ◽  
Feedback Loop ◽  
Negative Feedback Loop ◽  
Self Renewal ◽  
Hematopoietic Stem

scholarly journals Interrupted E2F1-miR-34c-SCF negative feedback loop by hyper-methylation promotes colorectal cancer cell proliferation

2016 ◽  
Vol 36 (1) ◽  
Author(s):  
Shu Yang ◽  
Bo Wu ◽  
Haimei Sun ◽  
Fengqing Ji ◽  
Tingyi Sun ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Cell Proliferation ◽  
Stem Cell ◽  
Cancer Cell ◽  
Negative Feedback ◽  
Stem Cell Factor ◽  
Feedback Loop ◽  
Colorectal Cancer Cell ◽  
Negative Feedback Loop ◽  
Cancer Cell Proliferation

E2F1 promoted miR-34c transcription which reduced its target stem cell factor (SCF) and inhibited colorectal cancer (CRC) cell proliferation. While, SCF increased E2F1 production, suggesting an existence of E2F1-miR-34c-SCF negative feedback loop, which was interrupted by hyper-methylation of miR-34c promoter in CRC cells.

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