Ethylene negatively regulates cold tolerance through HbEIN3-HbICE2 regulatory module in Hevea brasiliensis
文献类型: 外文期刊
作者: Zeng, Xue-Wei 1 ; Jiang, Wei-Zeng 1 ; Zhang, Jian-Long 1 ; Ding, Jia-Hui 1 ; Qiu, Yi-Min 1 ; Wen, Wei 1 ; Yang, Huan 1 ; Zhang, Qian-Yu 1 ; Yuan, Hong-Mei 1 ;
作者机构: 1.Hainan Univ, Sch Trop Agr & Forestry, Sanya Inst Breeding & Multiplicat, Natl Key Lab Trop Crop Breeding,Sch Breeding & Mul, Sanya 572025, Peoples R China
2.Chinese Acad Trop Agr Sci, Inst Trop Biosci & Biotechnol, Key Lab Banana Genet Improvement Hainan Prov, Haikou 571101, Peoples R China
期刊名称:PLANT PHYSIOLOGY AND BIOCHEMISTRY ( 影响因子:5.7; 五年影响因子:6.4 )
ISSN: 0981-9428
年卷期: 2025 年 219 卷
页码:
收录情况: SCI
摘要: Cold stress can result in reduced growth rates, decreased latex production, and restricted areas for the Para rubber tree ( Hevea brasiliensis). However, the molecular mechanisms governing the response of Hevea brasiliensis to cold stress remain elusive. Here, we found that ethylene plays a negative role in Hevea brasiliensis responses to cold stress. Treatment with the ethylene synthesis precursor 1-aminocyclopropane-1-carboxylic acid (ACC) decreased the cold tolerance of Hevea brasilien sis, while exogenous treatment with Ag+ (an ethylene signal inhibitor) had the opposite effect. Additionally, overexpressing HbE IN3 decreased cold stress tolerance in Arabidopsis and Taraxacum koksaghyz plants. Quantitative real-time PCR analysis indicated that HbEIN3-1 and HbEIN3-2 repress the expression of the cold-responsive genes HbCBF1-3 in Hevea brasiliensis. Moreover, HbEIN3-1 and HbEIN3-2 directly bind to the HbC BF1 promoter to suppress its transcription. Further investigation revealed that HbEIN3s interact with and dampen the transcriptional activity of HbICE2, a crucial transcription factor that positively regulates the cold signaling pathway, thereby attenuating the expression of HbICE2-targeted genes. Collectively, these findings indicate that HbEIN3s play a crucial role in ethylene- regulated cold tolerance through the repression of HbC BF1 expression and HbICE2 transcriptional activity.
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