Damage activates <i>EXG1</i> and <i>RLP44</i> to suppress vascular differentiation during regeneration in <i>Arabidopsis</i>. Mazumdar, S., Augstein, F., Zhang, A., Musseau, C., Anjam, M. S., Marhavy, P., & Melnyk, C. W. Plant Communications, 6(4):101256, April, 2025.
Damage activates <i>EXG1</i> and <i>RLP44</i> to suppress vascular differentiation during regeneration in <i>Arabidopsis</i> [link]Paper  doi  abstract   bibtex   
Plants possess remarkable regenerative abilities to form de novo vasculature after damage and in response to pathogens that invade and withdraw nutrients. To identify common factors that affect vascular formation upon stress, we searched for Arabidopsis thaliana genes differentially expressed upon Agrobacterium infection, nematode infection, and plant grafting. One such gene is cell wall-related and highly induced by all three stresses, which we named ENHANCED XYLEM AND GRAFTING1 (EXG1), since its mutations promote ectopic xylem formation in a vascular cell induction system and enhance graft formation. Further observations revealed that exg1 mutants show inhibited cambium development and callus formation but enhanced tissue attachment, syncytium size, phloem reconnection, and xylem formation. Given that brassinosteroids also promote xylem differentiation, we analyzed brassinosteroid-related genes and found that mutations in RLP44 encoding a receptor-like protein cause similar regeneration-related phenotypes as mutations in EXG1. Like EXG1, RLP44 expression is also induced by grafting and wounding. Mutations in EXG1 and RLP44 affect the expression of many genes in common, including those related to cell walls and genes important for vascular regeneration. Our results suggest that EXG1 integrates information from wounding or pathogen stress and functions with RLP44 to suppress vascular differentiation during regeneration and healing.
@article{mazumdar_damage_2025,
	title = {Damage activates \textit{{EXG1}} and \textit{{RLP44}} to suppress vascular differentiation during regeneration in \textit{{Arabidopsis}}},
	volume = {6},
	issn = {2590-3462},
	url = {https://www.sciencedirect.com/science/article/pii/S2590346225000185},
	doi = {10.1016/j.xplc.2025.101256},
	abstract = {Plants possess remarkable regenerative abilities to form de novo vasculature after damage and in response to pathogens that invade and withdraw nutrients. To identify common factors that affect vascular formation upon stress, we searched for Arabidopsis thaliana genes differentially expressed upon Agrobacterium infection, nematode infection, and plant grafting. One such gene is cell wall-related and highly induced by all three stresses, which we named ENHANCED XYLEM AND GRAFTING1 (EXG1), since its mutations promote ectopic xylem formation in a vascular cell induction system and enhance graft formation. Further observations revealed that exg1 mutants show inhibited cambium development and callus formation but enhanced tissue attachment, syncytium size, phloem reconnection, and xylem formation. Given that brassinosteroids also promote xylem differentiation, we analyzed brassinosteroid-related genes and found that mutations in RLP44 encoding a receptor-like protein cause similar regeneration-related phenotypes as mutations in EXG1. Like EXG1, RLP44 expression is also induced by grafting and wounding. Mutations in EXG1 and RLP44 affect the expression of many genes in common, including those related to cell walls and genes important for vascular regeneration. Our results suggest that EXG1 integrates information from wounding or pathogen stress and functions with RLP44 to suppress vascular differentiation during regeneration and healing.},
	number = {4},
	urldate = {2025-04-22},
	journal = {Plant Communications},
	author = {Mazumdar, Shamik and Augstein, Frauke and Zhang, Ai and Musseau, Constance and Anjam, Muhammad Shahzad and Marhavy, Peter and Melnyk, Charles W.},
	month = apr,
	year = {2025},
	keywords = {Cell wall, Grafting, Regeneration, Stress, Wounding, Xylem, cell wall, grafting, regeneration, stress, wounding, xylem},
	pages = {101256},
}

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