CLAVATA modulates auxin homeostasis and transport to regulate stem cell identity and plant shape in a moss

PpRPK2 modulates auxin homeostasis and transport to specify stem cell identity and plant shape in the moss Physcomitrella

10.1101/2021.06.24.449551 ◽

2021 ◽

Author(s):

Zoe Nemec Venza ◽

Connor Madden ◽

Amy Stewart ◽

Wei Liu ◽

Ondrej Novak ◽

...

Keyword(s):

Stem Cell ◽

Cell Function ◽

Cell Activity ◽

Fundamental Property ◽

Land Plant ◽

Cell Identity ◽

Auxin Homeostasis ◽

Plant Stem ◽

Plant Form ◽

Hormone Homeostasis

Plant shape is determined by the activity of stem cells in the growing tips, and evolutionary changes in shape are linked to changes in stem cell function. The CLAVATA pathway is a key regulator of stem cell function in the multicellular shoot tips of Arabidopsis, acting via the WUSCHEL transcription factor to modulate hormone homeostasis. Broad scale evolutionary comparisons have shown that CLAVATA is a conserved regulator of land plant stem cell function, but CLAVATA acts independently of WUSCHEL-like (WOX) proteins in bryophytes, raising questions about the evolution of stem cell function and the role of the CLAVATA pathway. Here we show that the moss (Physcomitrella) CLAVATA pathway affects stem cell activity and overall plant shape by modulating hormone homeostasis. CLAVATA pathway components are expressed in the tip cells of filamentous tissues, regulating cell identity, filament branching patterns and plant spread. The PpRPK2 receptor-like kinase plays the major role and is expressed more strongly than other receptor-encoding genes. Pprpk2 mutants have abnormal responses to cytokinin, and auxin transport inhibition and show reduced PIN auxin transporter expression. We propose a model whereby PpRPK2 modulates PIN activity to determine stem cell identity and overall plant form in Physcomitrella. Our data indicate that CLAVATA-mediated auxin homeostasis is a fundamental property of plant stem cell function likely exhibited by the last shared common ancestor of land plants.

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Faculty Opinions recommendation of AP2-type transcription factors determine stem cell identity in the moss Physcomitrella patens.

Faculty Opinions – Post-Publication Peer Review of the Biomedical Literature ◽

10.3410/f.717952920.793458475 ◽

2012 ◽

Author(s):

Renze Heidstra

Keyword(s):

Stem Cell ◽

Transcription Factors ◽

Physcomitrella Patens ◽

Cell Identity

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Faculty Opinions recommendation of Mitochondrial dynamics impacts stem cell identity and fate decisions by regulating a nuclear transcriptional program.

Faculty Opinions – Post-Publication Peer Review of the Biomedical Literature ◽

10.3410/f.726388238.793520395 ◽

2016 ◽

Author(s):

Vijay Tiwari ◽

Amitava Basu

Keyword(s):

Stem Cell ◽

Mitochondrial Dynamics ◽

Transcriptional Program ◽

Cell Identity

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Heat Shock Alters Mesenchymal Stem Cell Identity and Induces Premature Senescence

Frontiers in Cell and Developmental Biology ◽

10.3389/fcell.2020.565970 ◽

2020 ◽

Vol 8 ◽

Author(s):

Chen Shimoni ◽

Myah Goldstein ◽

Ivana Ribarski-Chorev ◽

Iftach Schauten ◽

Dana Nir ◽

...

Keyword(s):

Stem Cell ◽

Heat Shock ◽

Mesenchymal Stem Cell ◽

Premature Senescence ◽

Cell Identity

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Set1 Targets Genes with Essential Identity and Tumor-Suppressing Functions in Planarian Stem Cells

Genes ◽

10.3390/genes12081182 ◽

2021 ◽

Vol 12 (8) ◽

pp. 1182

Author(s):

Prince Verma ◽

Court K. M. Waterbury ◽

Elizabeth M. Duncan

Keyword(s):

Stem Cells ◽

Stem Cell ◽

Mammalian Cells ◽

Cell Function ◽

Genotoxic Stress ◽

Specific Gene ◽

Cell Identity ◽

Chromatin Signature ◽

Lysine Methyltransferase

Tumor suppressor genes (TSGs) are essential for normal cellular function in multicellular organisms, but many TSGs and tumor-suppressing mechanisms remain unknown. Planarian flatworms exhibit particularly robust tumor suppression, yet the specific mechanisms underlying this trait remain unclear. Here, we analyze histone H3 lysine 4 trimethylation (H3K4me3) signal across the planarian genome to determine if the broad H3K4me3 chromatin signature that marks essential cell identity genes and TSGs in mammalian cells is conserved in this valuable model of in vivo stem cell function. We find that this signature is indeed conserved on the planarian genome and that the lysine methyltransferase Set1 is largely responsible for creating it at both cell identity and putative TSG loci. In addition, we show that depletion of set1 in planarians induces stem cell phenotypes that suggest loss of TSG function, including hyperproliferation and an abnormal DNA damage response (DDR). Importantly, this work establishes that Set1 targets specific gene loci in planarian stem cells and marks them with a conserved chromatin signature. Moreover, our data strongly suggest that Set1 activity at these genes has important functional consequences both during normal homeostasis and in response to genotoxic stress.

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Histone Acetyltransferases and Stem Cell Identity

Cancers ◽

10.3390/cancers13102407 ◽

2021 ◽

Vol 13 (10) ◽

pp. 2407

Author(s):

Ruicen He ◽

Arthur Dantas ◽

Karl Riabowol

Keyword(s):

Stem Cells ◽

Stem Cell ◽

Cell Fate ◽

Epigenetic Modification ◽

Cell Types ◽

Histone Acetyltransferases ◽

Specific Cell ◽

Cell Fates ◽

Cell Identity ◽

Hematopoietic Stem

Acetylation of histones is a key epigenetic modification involved in transcriptional regulation. The addition of acetyl groups to histone tails generally reduces histone-DNA interactions in the nucleosome leading to increased accessibility for transcription factors and core transcriptional machinery to bind their target sequences. There are approximately 30 histone acetyltransferases and their corresponding complexes, each of which affect the expression of a subset of genes. Because cell identity is determined by gene expression profile, it is unsurprising that the HATs responsible for inducing expression of these genes play a crucial role in determining cell fate. Here, we explore the role of HATs in the maintenance and differentiation of various stem cell types. Several HAT complexes have been characterized to play an important role in activating genes that allow stem cells to self-renew. Knockdown or loss of their activity leads to reduced expression and or differentiation while particular HATs drive differentiation towards specific cell fates. In this study we review functions of the HAT complexes active in pluripotent stem cells, hematopoietic stem cells, muscle satellite cells, mesenchymal stem cells, neural stem cells, and cancer stem cells.

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