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PpCSC1, a Novel ERD4 ortholog from Physcomitrium patens, plays a negative role in salt stress tolerance

Lu Chen1,2,#, Zhijie Ren2,#, Guangmin Zhao2, Xuan He2, Legong Li2, Sheng Teng1,*, Yikun He2,*, Fang Bao2,*
1 Key Laboratory of Microbiological Metrology, Measurement & Bio-product Quality Security, State Administration for Market Regulation, College of Life Sciences, China Jiliang University, 258 Xueyuan Street, Hangzhou, 310018, China
2 College of Life Sciences, Capital Normal University, 105 West Third Ring North Road, Beijing, 100048, China
* Corresponding Author: Sheng Teng. Email: email; Yikun He. Email: email; Fang Bao. Email: email
# These authors contributed equally to this work
(This article belongs to the Special Issue: Plant Responses to Abiotic Stress Mechanisms)

Phyton-International Journal of Experimental Botany https://doi.org/10.32604/phyton.2025.073817

Received 26 September 2025; Accepted 15 December 2025; Published online 26 December 2025

Abstract

ERD4 proteins, members of the early responsive-to-dehydration family, act as plasma membrane ion channels that contribute to ion homeostasis and modulate plant response to abiotic stresses. However, the functions of ERD4 homologs in non-vascular species remain largely unexplored. Here, we characterized an ERD4 family homolog in Physcomitrium patens (Hedw.) Mitt., PpCSC1 (Calcium-permeable Stress-responsive Cation Channel 1), and investigated its role in salt stress response. PpCSC1 localized to the plasma membrane and functioned as a non-selective cation channel permeable to Na+, K+, Ca2+, and Mg2+. Under salt treatment, PpCSC1 transcripts were markedly downregulated, whereas overexpression lines exhibited enhanced salt sensitivity. Ion content analysis further revealed reduced K+ accumulation, lowered K+/Na+ ratios, and elevated Mg2+ levels, collectively disrupting ionic homeostasis and impairing salt tolerance. Transcriptional regulation analysis revealed that the C2H2-type zinc finger transcription factor PpSTOP2 directly activated PpCSC1 expression. Notably, PpSTOP2 knockout plants displayed reduced PpCSC1 mRNA accumulation and improved salt tolerance. Together, these findings indicate that PpCSC1 is a plasma membrane-localized cation channel that negatively regulates salt tolerance by disturbing ion balance, and that its regulation by PpSTOP2 integrates upstream signaling with downstream physiological responses. This work provides new insight into how non-selective ion channels shape stress adaptation in early land plants.

Keywords

Physcomitrium patens; Calcium-permeable Stress-responxive Cation Channel 1 (PpCSC1); cation transport activity; salt stress; transcriptional regulation
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