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橡胶树排胶障碍是制约全球橡胶种植园发展的主要因素,它是由以下两个不同病症导致的:(1)割面干涸(TPD)-过度割胶引起的可逆生理反应,(2)割面树皮坏死(BN)-由橡胶树根颈韧皮部扩展的不可逆病变。树皮坏死(BN)目前危害了世界大部分胶园,胶园受害严重度取决于橡胶品种、树龄、种植地和种植地区。橡胶树树皮病的多态性一直是一个有争议的问题,通过对许多胶园的调研,该问题最近得到了解决。虽然前期和最近的病原分析不具决定性,但是环境因素却显示出同树皮坏死有联系。在对近期开割的胶园进行流行病调查,发现早期患病胶树地点呈非随机性。这些易发病区主要靠近沼泽地、路旁、风干行、原推土机过道、树林树桩残余地和斜坡缓冲地段的附近区域。在树皮坏死发生区,虽然没有发现与土壤化学因素有明显的关系,但是,土壤物理分析(如透度法)却表明,土壤的较高紧实度常同患病胶树的根系生长较弱有关联。另外,通常在芽接点接合处可以很好地观察到树皮坏死早期症状。通过PMS压力室获得的大量可比生态生理的测量数据显示,患病胶树呈现水分协迫特征,意味着病树树干同其根系存在着一种非理想的维管关系。因此,同土壤紧实度相关的土壤缺水状况、旱季不能满足胶树水分需求的脆弱根系、被扰乱的树液流动和土壤排水等因素的共同作用,被怀疑是诱导树干接芽区树皮坏死(坏死向上扩展到割面) 生理的一个主要外部诱因。在这些协迫的作用下,细胞与分子研究显示,橡胶树生理失调是导致树皮坏死迅速扩展的原因。在这些协迫的作用下,在胶树芽接部位的细胞破裂,释放极具扩散性的高浓度氰化物。在患病胶树的韧皮部生氰和解氰活动的极不协调,以及氰化物的释放,导致其周围的细胞受到毒害。最后, 这样一种多学科的研究方法为由协迫诱导的多因素生理病害研究提供了一个完整的新模式。
Barrier rubber gum disorder is the main factor restricting the development of the global rubber plantation, which is caused by two different conditions: (1) TPD - reversible physiological reaction caused by over-excision, (2) cut tree Skin necrosis (BN) - An irreversible lesion that expands through the rubber tree root collar phloem. Bark necrosis (BN) is currently endangering most of the rubber plantations in the world. The severity of the rubber plantations depends on the rubber species, age, planting and planting areas. Polymorphism of rubber tree bark has always been a matter of debate, which has recently been resolved through research on many rubber plantations. Although previous and recent pathogen analyzes are inconclusive, environmental factors have been shown to be associated with bark necrosis. In the recent opening of the rubber plant for epidemiological investigation and found that the location of the early ill rubber tree was non-random. These areas are predominantly located near wetlands, roadsides, air-dry lines, former bulldozer aisles, remnants of tree stumps and areas near the buffer zone. In the bark necrosis area, although no obvious relationship was found with the soil chemical factors, soil physical analysis (such as the permeability method) showed that the higher compaction of the soil was often associated with the growth of the diseased gum tree Weakly related. In addition, early symptoms of bark necrosis are usually well observed at the bud junction junctions. A large number of comparable ecophysiological measurements obtained from PMS pressure chambers show that the diseased gum tree exhibits a water-forcing characteristic, suggesting a non-ideal vascular relationship between the diseased tree trunk and its root system. Therefore, soil water deficit associated with soil compaction, fragile roots that can not meet the water requirement of gum trees during the dry season, disturbed flow of sap and soil drainage are all suspected to be responsible for the induction of bark Necrosis (necrosis extending up to the cut surface) is a major external incentive for physiology. Under these co-ordinated efforts, cellular and molecular studies have shown that the physiological disturbance of the rubber tree is responsible for the rapid expansion of bark necrosis. Under these synergistic effects, the cells in the budding junctions of the gum tree break down and release very high concentrations of cyanide. The extremely uncoordinated activities of cyanide and decyanation in the phloem of diseased gum trees and the release of cyanide lead to the poisoning of the surrounding cells. Finally, such a multidisciplinary approach provides a complete new paradigm for co-induced multifactorial physiological disease research.