This study investigated the endogenous phytosulfokine α (PSKα) signaling during opening and senescence in rose flowers. Our results showed that the higher phytosulfokines (PSKs) and tyrosyl protein sulfotransferase (TPST) expression could be responsible for higher endogenous PSKα accumulation in petals during rose flowers opening (stages 2 and 3). By triggering the endogenous PSKα signaling, higher phytosulfokine receptor 1 (PSKR1) expression could be responsible for higher cytosolic cyclic guanosine monophosphate (cGMP) accumulation in petals during rose flowers opening (stages 3 and 4). Higher protein kinase G (PKG) and cyclic nucleotide-gated ion channel 1 (CNGC1) expression accompanying higher plasma membrane intrinsic protein 2 (PIP2) and tonoplast intrinsic protein 1 (TIP1) expression in petals during rose flowers opening may arise from higher cytosolic cGMP accumulation giving rise to higher petals relative water content (RWC) (stage 4). Triggering phosphodiesterase (PDE) expression lay off cytosolic cGMP signaling. Suppressing PKG and CNGC1 expression accompanying lower PIP2 and TIP1 expression accelerates petals senescence in rose flowers representing by deteriorating petals membrane integrity revealed by higher electrolyte leakage and malondialdehyde (MDA) accumulation (stage 5 and 6). For delaying petals senescence and prolonging vase life in cut rose flowers, we employed exogenous PSKα treatment at the commercial harvest stage (stage 3). Our results showed that the suppressing PDE expression in petals by exogenous 150 nM PSKα treatment could be responsible for allowing cytosolic cGMP signaling ongoing for supporting PKG and CNGC1 expression accompanying by higher PIP2 and TIP1 expression. Exogenous 150 nM PSKα treatment, outperforming cut rose flowers by delayed senescence and prolonged vase life to 16 days from 12 days could be ascribed to preserving membrane integrity revealed by lower electrolyte leakage and MDA accumulation. Our results could be proposed that exogenous PSKα treatment and endogenous PSKα signaling for employing in the floriculture industry for delaying petals senescence and prolonging the vase life of cut rose flower.

本研究调查了月季花开放和衰老过程中的内源性植物磺化因子 α (PSKα) 信号。我们的结果表明，较高的植物磺化因子( PSK ) 和酪氨酰蛋白磺基转移酶 ( TPST ) 表达可能是月季花开放期间（第 2 和第 3 阶段）花瓣中较高的内源性 PSKα 积累的原因。通过触发内源性 PSKα 信号传导，较高的植物磺化因子受体 1 ( PSKR1 ) 表达可能是月季花开放期间花瓣中较高的胞质环磷酸鸟苷 (cGMP) 积累的原因（第 3 和第 4 阶段）。高级蛋白激酶 G ( PKG ) 和环核苷酸门控离子通道 1 ( CNGC1) 伴随着更高的质膜内在蛋白 2 ( PIP2 ) 和液泡膜内在蛋白 1 ( TIP1 ) 在玫瑰花开放期间在花瓣中表达的表达可能是由于更高的胞质 cGMP 积累导致更高的花瓣相对含水量 (RWC)（阶段 4）。触发磷酸二酯酶 ( PDE ) 表达会解除胞质 cGMP 信号传导。抑制伴随较低PIP2和TIP1 的PKG和CNGC1表达表达加速玫瑰花中的花瓣衰老，表现为更高的电解质泄漏和丙二醛 (MDA) 积累（第 5 和第 6 阶段）揭示的花瓣膜完整性恶化。为了延缓玫瑰切花的花瓣衰老和延长瓶插寿命，我们在商业收获阶段（第 3 阶段）采用外源 PSKα 处理。我们的结果表明，外源性 150 nM PSKα 处理抑制花瓣中的PDE表达可能是导致细胞溶质 cGMP 信号持续支持PKG和CNGC1表达的原因，伴随着更高的PIP2和TIP1表达。外源性 150 nM PSKα 处理，通过延迟衰老和将花瓶寿命从 12 天延长至 16 天而优于切开的月季花，可归因于通过较低的电解质泄漏和 MDA 积累来保持膜完整性。我们的研究结果表明，外源性 PSKα 处理和内源性 PSKα 信号可用于花卉业，以延缓花瓣衰老并延长切花玫瑰花的瓶插寿命。