DISEASE LESION MIMICS IN MAIZE .1. EFFECT OF GENETIC BACKGROUND, TEMPERATURE, DEVELOPMENTAL AGE, AND WOUNDING ON NECROTIC SPOT FORMATION WITH LES1
DISEASE LESION MIMICS IN MAIZE .1. EFFECT OF GENETIC BACKGROUND, TEMPERATURE, DEVELOPMENTAL AGE, AND WOUNDING ON NECROTIC SPOT FORMATION WITH LES1
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DOI：
10.1016/0012-1606(82)90125-7
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发表时间：
1982-01-01
影响因子：
2.7
通讯作者：
WALBOT, V
中科院分区：
文献类型：
--
作者：
HOISINGTON, DA;NEUFFER, MG;WALBOT, V
Les 1是玉米（Z. mays L.），导致产生坏死的叶斑。该性状的表达是温度敏感的，并且不允许表达的温度由基因所处的遗传背景决定。在非允许条件下暴露24-48小时将在最敏感的基因型中诱导损伤产生。病变从叶尖（叶子最古老的部分）开始，并通过完全膨胀的组织向基瓣发展。从在允许或非允许温度下生长并置于水、GA或脱落酸溶液中的植物切下的叶在20或30 ℃下均不形成新的损伤。C，叶片迅速衰老。然而，当将从正常和Les 1植物上切下的叶子置于激动素中时，衰老被延迟，并且在20 ° C下出现许多损伤。C在Les 1植物上。有一个发育时间窗口，在此期间玉米叶细胞可以被诱导形成病变：细胞必须完全伸长，但尚未衰老。这一假设是加强观察针刺伤害的叶子诱导病变只在一个乐队的组织。比目前产生病变的叶片面积小2天。Les 1在引起离散病变形成的行动的各种模型进行了讨论。
Les1, a dominant gene of maize (Z. mays L.), results in the production of necrotic leaf spots. Expression of this trait is temperature sensitive, and the nonpermissive temperature for expression is determined by the genetic background in which the gene is placed. Exposure to nonpermissive conditions for 24-48 h will induce lesion production in the most sensitive genotype. Lesions from first at the leaf tip, the oldest part of the leaf, and progress basipetally through fully expanded tissue. Leaves excised from plants grown at either permissive or nonpermissive temperatures and placed in water, GA, or abscisic acid solutions form no new lesions at either 20 or 30.degree. C, and the leaves senesce rapidly. However, when leaves excised from normal and Les1 plants are placed in kinetin, senescence is delayed and numerous lesions develop at 20.degree. C on Les1 plants. There is a developmental time window during which maize leaf cells can be induced to form lesions: cells must be fully elongated but not yet senescent. This hypothesis is strengthened by the observation that pinprick wounding of leaves induces lesions only in a band of tissue .apprx. 2 days younger than the area of the leaf currently producing lesions. Various models for the action of Les1 in causing discrete lesion formation are discussed.