SC35-mediated bZIP49 splicing regulates K⁺ channel AKT1 for salt stress adaptation in poplar
Xiao Liu, Yu Bao, Manyu Zhang, Han Zhang, Meng‐Xue Niu, Shujing Liu, Meiying Liu, Mengbo Huang, Chao Liu, Weilun Yin, Hou‐Ling Wang, Xinli Xia
Abstract
Soil salinization threatens plant distribution, crop yields, and ecosystem stability. In response, plants activate potassium (K+) signaling to maintain Na⁺/K⁺ balance, though the mechanisms regulating K⁺ uptake under salt stress remain poorly understood. This study identified two splice variants of the bZIP49 transcription factor in Populus tomentosa: unspliced “bZIP49L” and spliced “bZIP49S”. bZIP49S, the active form under salt stress, reduces salt tolerance when overexpressed, while bzip49cr knockout enhances it. The serine/arginine-rich splicing factor SC35 was identified as a regulator of bZIP49 mRNA splicing through a self-developed experimental method, and its overexpression enhances salt sensitivity. bZIP49S inhibits the K+ transporter AKT1 by binding its promoter, and AKT1 loss in bzip49cr mutant limits K+ influx and reduces salt tolerance. Under salt stress, the E2 ubiquitin-conjugating enzyme UBC32 promotes SC35 degradation via ubiquitination, lowering bZIP49S levels and alleviating the inhibition of AKT1. This facilitates K⁺ uptake, restores Na⁺/K⁺ balance, and improves salt tolerance. Our study highlights the critical role of bZIP49 splicing and the “UBC32-SC35-bZIP49-AKT1” module in modulating Na⁺/K⁺ balance under salt stress in poplar. This study identifies a regulatory module in which UBC32 and SC35 regulate bZIP49 splicing to maintain potassium balance, revealing how poplar adapts to salt stress and providing new insights into plant responses to soil salinity.