Núcleo de Biotecnologia, Universidade Federal do Espírito Santo, Vitória, ES, 29040-090, Brazil.
Núcleo Multidisciplinar de Pesquisa em Biologia, Universidade Federal do Rio de Janeiro, Duque de Caxias, RJ, 25240-005, Brazil.
Plant Cell Rep. 2024 Oct 23;43(11):269. doi: 10.1007/s00299-024-03358-w.
The proteomic analysis of PMeV-complex-infected C. papaya unveiled proteins undergoing modulation during the plant's development. The infection notably impacted processes related to photosynthesis and cell wall dynamics. The development of Papaya Sticky Disease (PSD), caused by the papaya meleira virus complex (PMeV-complex), occurs only after the juvenile/adult transition of Carica papaya plants, indicating the presence of tolerance mechanisms during the juvenile development phase. In this study, we quantified 1609 leaf proteins of C. papaya using a label-free strategy. A total of 345 differentially accumulated proteins were identified-38 at 3 months (juvenile), 130 at 4 months (juvenile/adult transition), 160 at 7 months (fruit development), and 17 at 9 months (fruit harvesting)-indicating modulation of biological processes at each developmental phase, primarily related to photosynthesis and cell wall remodeling. Infected 3- and 4-mpg C. papaya exhibited an accumulation of photosynthetic proteins, and chlorophyll fluorescence results suggested enhanced energy flux efficiency in photosystems II and I in these plants. Additionally, 3 and 4-mpg plants showed a reduction in cell wall-degrading enzymes, followed by an accumulation of proteins involved in the synthesis of wall precursors during the 7 and 9-mpg phases. These findings, along with ultrastructural data on laticifers, indicate that C. papaya struggles to maintain the integrity of laticifer walls, ultimately failing to do so after the 4-mpg phase, leading to latex exudation. This supports initiatives for the genetic improvement of C. papaya to enhance resistance against the PMeV-complex.
番木瓜环斑病毒复合侵染引起的番木瓜蛋白质组分析揭示了植物发育过程中发生调节的蛋白质。该感染显著影响了与光合作用和细胞壁动态相关的过程。番木瓜贴梗果病毒复合（PMeV-complex）引起的番木瓜贴梗果病（PSD）仅在 Carica papaya 植物幼龄/成年过渡期后发生，表明在幼龄发育阶段存在耐受机制。在这项研究中，我们使用无标记策略对番木瓜的 1609 种叶蛋白进行了定量分析。共鉴定出 345 种差异积累蛋白，其中 38 种在 3 个月（幼龄），130 种在 4 个月（幼龄/成年过渡期），160 种在 7 个月（果实发育），17 种在 9 个月（果实收获），表明每个发育阶段的生物过程都发生了调节，主要与光合作用和细胞壁重塑有关。感染的 3-和 4-mpg 番木瓜积累了光合作用蛋白，叶绿素荧光结果表明这些植物中的光合系统 II 和 I 的能量通量效率增强。此外，3-和 4-mpg 植物中的细胞壁降解酶减少，随后在 7-和 9-mpg 阶段积累了参与细胞壁前体合成的蛋白。这些发现，以及乳管的超微结构数据，表明番木瓜难以维持乳管壁的完整性，最终在 4-mpg 阶段后无法维持，导致乳胶渗出。这支持了对番木瓜进行遗传改良以提高对 PMeV-complex 抗性的倡议。
