The Arabidopsis () root epidermis consists of a position-dependent pattern of root hair cells and non-hair cells. Underlying this cell type patterning is a network of transcription factors including a central MYB-basic helix-loop-helix-WD40 complex containing WEREWOLF (WER), GLABRA3 (GL3)/ENHANCER OF GLABRA3, and TRANSPARENT TESTA GLABRA1. In this study, we used a genetic enhancer screen to identify , a mutant allele of the ribosome biogenesis factor (RBF) gene (), which caused prospective root hair cells to instead adopt the non-hair cell fate. We discovered that this cell fate switch relied on MYB23, a MYB protein encoded by a WER target gene and acting redundantly with WER. In the mutant, exhibited ectopic expression that was WER independent and instead required ANAC082, a recently identified ribosomal stress response mediator. We examined additional RBF mutants that produced ectopic non-hair cells and determined that this cell fate switch is generally linked to defects in ribosome biogenesis. Furthermore, the flagellin peptide flg22 triggers the ANAC082-MYB23-GL2 pathway. Taken together, our study provides a molecular explanation for root epidermal cell fate switch in response to ribosomal defects and, more generally, it demonstrates a novel regulatory connection between stress conditions and cell fate control in plants.
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http://dx.doi.org/10.1105/tpc.19.00773 | DOI Listing |
Nat Rev Immunol
January 2025
Stem Cells and Regenerative Medicine Center, Baylor College of Medicine, Houston, TX, USA.
Fate decisions during immune cell development require temporally precise changes in gene expression. Evidence suggests that the dynamic modulation of these changes is associated with the formation of diverse, membrane-less nucleoprotein assemblies that are termed biomolecular condensates. These condensates are thought to orchestrate fate-determining transcriptional and post-transcriptional processes by locally and transiently concentrating DNA or RNA molecules alongside their regulatory proteins.
View Article and Find Full Text PDFJ Adv Res
January 2025
the Second Affiliated Hospital, Guangzhou Medical University, Guangzhou 510260, China. Electronic address:
Introduction: Spinal cord injury (SCI) is a severe central nervous system disorder with limited treatment options. While autophagy plays a protective role in neural repair, its regulatory mechanisms in SCI remain unclear. Actin-like protein 6A (Actl6a) influences cell fate and neural development, yet its specific role in SCI repair is not well understood.
View Article and Find Full Text PDFCurr Opin Pharmacol
January 2025
Functional Genomics and Metabolism Research Unit, Department of Biochemistry and Molecular Biology, University of Southern Denmark, Campusvej 55, DK-5230, Odense, Denmark. Electronic address:
Chromatin dynamics, involving reversible changes in chromatin structure, shape key cellular processes and genomic integrity during development and proliferation, with disruptions leading to cancer. Histones, core components of chromatin and substrates for chromatin-modifying enzymes, play crucial roles in oncogenesis when misregulated or mutated. This is particularly pronounced in pediatric hind brain cancers, some of which are driven primarily by the oncohistone H3K27M and the recently identified oncohistone-mimic protein CXorf67/EZHIP.
View Article and Find Full Text PDFProc Natl Acad Sci U S A
February 2025
Division of Dermatology, Department of Medicine, Washington University School of Medicine, St. Louis, MO 63110.
Classical tissue recombination experiments demonstrate that cell-fate determination along the anterior-posterior axis of the Müllerian duct occurs prior to postnatal day 7 in mice. However, little is known about how these cell types are maintained in adults. In this study, we provide genetic evidence that a balance between antagonistic retinoic acid (RA) and estrogen signaling activity is required to maintain simple columnar cell fate in adult uterine epithelium.
View Article and Find Full Text PDFProc Natl Acad Sci U S A
February 2025
Pediatric Surgical Research Laboratories, Massachusetts General Hospital, Boston, MA 02114.
Anti-Müllerian hormone (AMH) protects the ovarian reserve from chemotherapy, and this effect is most pronounced with Doxorubicin (DOX). However, DOX toxicity and AMH rescue mechanisms in the ovary have remained unclear. Herein, we characterize the consequences of these treatments in ovarian cell types using scRNAseq.
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