Mertz S M, Arntzen C J
United States Department of Agriculture, Agricultural Research Service, Department of Botany, University of Illinois, Urbana, Illinois 61801.
Plant Physiol. 1977 Sep;60(3):363-9. doi: 10.1104/pp.60.3.363.
Pathotoxin preparations were obtained from either axenic culture filtrate of race T of Bipolaris maydis (Nisikado) Shoemaker (new culture media and toxin purification procedures are described) or extracts of maize leaves infected with the fungus. The toxins (10(-6) to 10(-8)m) caused inhibition of [(86)Rb]K(+) uptake in leaf discs and apical root segments of Zea mays L. cv W64A Texas (Tcms) and normal (N) cytoplasms. Significant inhibition was measurable as early as 5 min after adding toxin. In Tcms per cent inhibition was increased by increasing toxin concentration and time in toxin, by using solution at pH 5 rather than pH 7, by decreasing external KCl concentration over the range 50 to 0.1 mm (in the presence of 0.5 mm CaSO(4)), or by exposing leaf discs to light rather than dark during the uptake period in toxin. Root uptake of (22)Na(+) and (36)Cl(-) was inhibited to a lesser extent than K(+). Inhibition of (32)PO(4) (3-) uptake occurred after 40 min when cyclosis had ceased.When combined with data in the literature, our data indicate that the plasmalemma is the probable primary site of toxin action in N and Tcms maize. Comparison of the effects of toxin on K(+) uptake in N and Tcms maize suggests the existence of more than one mode of toxin action: a weak disruptive effect in N and Tcms, and in addition, specific membrane sites in Tcms involved in monovalent ion uptake.Six genotypes in N or Tcms cytoplasm which exhibited different degrees of disease susceptibility in the field showed a corresponding gradation of susceptibility to the toxin when a K(+) uptake bioassay was used. This correlation is strong evidence that the sites of toxin action affecting K(+) transport have characteristics closely related to cellular factors regulating susceptibility to fungal attack.
病理毒素制剂可从玉米小斑病菌(Nisikado)Shoemaker小种T的无菌培养滤液(描述了新的培养基和毒素纯化程序)或感染该真菌的玉米叶片提取物中获得。毒素(10⁻⁶至10⁻⁸m)可抑制玉米(Zea mays L. cv W64A Texas,不育细胞质(Tcms)和正常(N)细胞质)叶片圆片和根尖切段对[⁸⁶Rb]K⁺的吸收。早在添加毒素5分钟后就能检测到显著抑制。在Tcms中,通过增加毒素浓度和在毒素中的处理时间、使用pH 5而非pH 7的溶液、在50至0.1毫米范围内降低外部KCl浓度(在存在0.5毫米CaSO₄的情况下)或在毒素吸收期间将叶片圆片置于光照而非黑暗条件下,抑制百分比会增加。根对²²Na⁺和³⁶Cl⁻的吸收受到的抑制程度小于对K⁺的抑制。当胞质环流停止40分钟后,³²PO₄³⁻的吸收受到抑制。结合文献中的数据,我们的数据表明质膜可能是毒素在N和Tcms玉米中作用的主要位点。毒素对N和Tcms玉米中K⁺吸收的影响比较表明存在多种毒素作用模式:在N和Tcms中有微弱的破坏作用,此外,在Tcms中存在参与单价离子吸收的特定膜位点。在田间表现出不同程度病害易感性的N或Tcms细胞质中的六种基因型,当使用K⁺吸收生物测定法时,对毒素表现出相应的易感性等级。这种相关性有力地证明了影响K⁺转运的毒素作用位点具有与调节对真菌侵袭易感性的细胞因子密切相关的特征。