Yang Jie, Li Na, Li Ming, Yi Ran, Qiu Lina, Wang Kangning, Zhao Shuang, Ma Fengwang, Mao Ke
State Key Laboratory for Crop Stress Resistance and High-Efficiency Production/Shaanxi Key Laboratory of Apple, College of Horticulture, Northwest A & F University, Yangling, Shaanxi, 712100, China.
Adv Sci (Weinh). 2025 Jul;12(25):e2501524. doi: 10.1002/advs.202501524. Epub 2025 Apr 26.
Cold stress is a major environmental factor limiting crop yield, quality, and geographical distribution worldwide. The homeodomain-leucine zipper (HD-Zip) transcription factor (TF) family plays a role in regulating plant abiotic stress responses, but the underlying mechanisms remain unclear. A HD-Zip TF, MdHB7L, is identified as promoting cold tolerance in apple. MdHB7L interacts with MdICE1L, enhancing its transcriptional activation of MdCBFs, and directly binds to MdCBF promoters to activate their expression. Conversely, MdICE1L inhibits the direct binding of MdHB7L on MdCBF promoters, revealing that MdHB7L acts as a cofactor rather than a TF when interacting with MdICE1L. Using ChIP-seq and RNA-seq, MdHB7L is found to directly regulate the expression of several key genes involved in ROS scavenging and biosynthesis of anthocyanins, soluble sugars, and proline, thereby enhancing apple cold tolerance. The E3 ubiquitin ligase MdHOS1 negatively regulates cold tolerance by interacting with and mediating the degradation of MdHB7L and MdICE1L, with a preference for MdICE1L over MdHB7L. This preference inhibits the MdHOS1-MdHB7L interaction and stabilizes MdHB7L, allowing it to sustain the plant's cold response as a TF after MdICE1L degradation. These findings provide new insights into the dynamic plant response to cold stress mediated by the MdHB7L-MdICE1-MdHOS1 module.
低温胁迫是限制全球作物产量、品质和地理分布的主要环境因素。同源异型域-亮氨酸拉链(HD-Zip)转录因子(TF)家族在调节植物非生物胁迫响应中发挥作用,但其潜在机制仍不清楚。一种HD-Zip TF,MdHB7L,被鉴定为可促进苹果的耐寒性。MdHB7L与MdICE1L相互作用,增强其对MdCBFs的转录激活,并直接结合到MdCBF启动子上以激活它们的表达。相反,MdICE1L抑制MdHB7L与MdCBF启动子的直接结合,表明MdHB7L在与MdICE1L相互作用时作为辅因子而非TF发挥作用。通过ChIP-seq和RNA-seq分析发现,MdHB7L直接调控参与活性氧清除以及花青素、可溶性糖和脯氨酸生物合成的几个关键基因的表达,从而增强苹果的耐寒性。E3泛素连接酶MdHOS1通过与MdHB7L和MdICE1L相互作用并介导它们的降解来负调控耐寒性,且对MdICE1L的偏好高于MdHB7L。这种偏好抑制了MdHOS1-MdHB7L的相互作用并稳定了MdHB7L,使其在MdICE1L降解后能够作为TF维持植物的低温响应。这些发现为MdHB7L-MdICE1-MdHOS1模块介导的植物对低温胁迫的动态响应提供了新的见解。