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Disease Cycle, Development and Management of Sclerotinia Stem Rot of Potato

机译:马铃薯菌核病茎腐病的病程,发展与管理

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Potato is severely affected by Sclerotinia sclerotiorum in the US Pacific Northwest (PNW) and satisfactory disease management has not been achieved until recently. Recent research has given a better understanding of key epidemiological factors which has resulted in improved disease management in the PNW. This work reviews the epidemiology of Sclerotinia stem rot and highlights information that has led to the better management of the disease on potato. The primary source of inoculum of Sclerotinia sclerotiorum for potato in the Columbia Basin of the PNW are ascospores produced within potato fields or carried by wind currents from neighboring fields planted to winter cereals or other crops. Ascospores are ejected from apothecia and disseminated throughout the Columbia Basin over an extended time period. Immature apothecia generally first emerge at or shortly after row closure in potato fields in the Columbia Basin. Ascospores of S. sclerotiorum are incapable of direct infection of intact green potato tissues, and flower blossoms are crucial for infection and development of the disease in potato. Airborne ascospores are deposited on open potato blossoms still attached to the canopy. Infested flowers fall and are trapped on stems, usually leaf axils, or fall on the ground, and fungal mycelia then rapidly colonize the blossoms when humidity is high in the plant canopy. Ascospores are also deposited on senescent and dead plant material on the ground, germinate, and produce mycelium. Infection occurs shortly after contaminated blossoms become lodged on stems in the plant canopy, or after stems come in contact with contaminated fallen blossoms or decomposing plant tissues on the ground. Infection can occur within 3 days after contact of contaminated blossoms with green tissue. Lesions initially appear on potato stems 14 to 30 days after row closure and 12 to 20 days following full bloom of primary inflorescences of potato in the Columbia Basin. Significant levels of outcrossing sexual recombination have been found in the homothallic S. sclerotiorum population in the Pacific Northwest. Sclerotinia stem rot of potato is best managed by using an integrated approach of combining cultural practices that produce optimum plant foliar development without producing an excessive crop canopy, irrigation management to avoid excessive amounts of irrigation water, and timely applications of fungicides. Contaminated flower blossoms served as a bridge for infection and fungicides applied before contaminated blossoms drop on foliage most effectively reduce infections on stems. Improved disease management has been achieved by timing fungicides to coincide with full bloom of primary inflorescences.
机译:马铃薯在美国西北太平洋地区(PNW)受到菌核盘菌的严重影响,直到最近才实现令人满意的疾病管理。最近的研究使人们对关键的流行病学因素有了更好的了解,这导致了西北太平洋地区疾病管理的改善。这项工作回顾了核盘菌茎腐病的流行病学,并着重介绍了导致更好地管理马铃薯病害的信息。西北太平洋哥伦比亚盆地马铃薯的核盘菌菌种的主要接种物是在马铃薯田中产生的子囊孢子,或者是由来自附近田地的风流携带到冬季谷物或其他农作物上的子囊孢子。子囊孢子从角质层排出,并在很长一段时间内散布到整个哥伦比亚盆地。未成熟的萎缩症通常首先在哥伦比亚盆地的马铃薯田行关闭时或关闭后不久出现。核盘菌的子囊孢子不能直接感染完整的绿色马铃薯组织,而花朵开花对于马铃薯疾病的感染和发展至关重要。空气中的子囊孢子沉积在仍然附着在树冠上的开放马铃薯花上。受侵染的花朵落下并被困在茎(通常是叶腋)上或落在地面上,然后当植物冠层湿度很高时,真菌菌丝体会迅速在花朵上定植。子囊孢还沉积在地面上的衰老和死植物材料上,发芽并产生菌丝体。在受污染的花朵堆积在植物冠层的茎上之后,或者在茎与受污染的下落的花朵接触或分解地面上的植物组织之后不久,就会发生感染。感染的花朵与绿色组织接触后3天内会发生感染。在行关闭后14至30天和哥伦比亚盆地马铃薯初生花序盛放后12至20天,病变最初出现在马铃薯茎上。在西北太平洋地区的同型S. sclerotiorum种群中发现了显着水平的异性重组。马铃薯的核盘菌茎腐病最好通过综合培养方法来综合管理,这些方法可以在不产生过多作物冠层的情况下产生最佳的植物叶发育,并进行灌溉管理以避免过多的灌溉水,并及时施用杀真菌剂。被污染的花朵可以作为感染的桥梁,在被污染的花朵掉落到叶子上之前,可以使用杀真菌剂来最有效地减少茎上的感染。通过选择杀菌剂使其与初生花序盛开同时进行,可以改善疾病管理。

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