Developmental genetics of mutants that specify knotted leaves in maize.

Of seven dominant knotted-leaf mutants tested, six mapped at or near Kn1 on the long arm of chromosome 1, and one was not linked to Kn1. Comparisons of phenotypes among these mutants allowed us to focus on a systematic abnormality: the parenchyma cells associated with lateral veins do not fully differentiate into bundle sheath, mesophyll or upper sclerenchyma. The more dramatic expression of Kn1 mutants-knots, ligule alterations and twisting-is sporadic and dependent on the time when the mutant acts in leaf primordium development. Using lw to mark leaf sectors that lose Kn1 following X-irradiation, we show that the knotted-leaf phenotype encoded by chromosome 1L is autonomous. Analysis of sectors lacking a particular Kn1 gene ( Kn1-N2) suggests that Kn1 itself, rather than a linked modifier gene, is autonomous in the leaf primordium. Aneuploid studies using various translocations involving 1L and marked by Adh1 allozymes are compared. The Kn1 mutant appears to encode a "new" function or a considerable overproduction of an extant product in the leaf. Kn1/- 1L hypoploids either express knotted poorly or not at all; transvection is ruled out, but the cause for this modification of Kn1 expression is not yet known.-Our working hypothesis is that Kn1 mutants permit the expression of a product that is usually not produced in leaf primordial cells. We suggest that this product interferes with the early cell-type commitments of cells near lateral veins. Thus, relatively uncommitted cells are present in more mature blades, where they may divide unexpectedly into knots or may induce bits of ligule.

在测试的7个显性扭叶突变体中，6个定位于1号染色体长臂上Kn1位点或其附近，1个与Kn1不连锁。对这些突变体表型的比较使我们能够聚焦于一种系统性异常：与侧脉相关的薄壁细胞无法完全分化为维管束鞘、叶肉或上部厚壁组织。Kn1突变体更显著的表现——扭结、叶舌改变和扭曲——是偶发的，且取决于突变在叶原基发育过程中发挥作用的时间。利用lw标记经X射线照射后失去Kn1的叶区域，我们发现1L染色体编码的扭叶表型具有自主性。对缺失特定Kn1基因（Kn1 - N2）区域的分析表明，在叶原基中具有自主性的是Kn1本身，而非与其连锁的修饰基因。我们对利用涉及1L且以Adh1等位酶为标记的各种易位进行的非整倍体研究进行了比较。Kn1突变体似乎编码了一种“新”功能，或者在叶片中大量过量产生了一种现有产物。Kn1 / - 1L亚倍体要么扭叶表型表达较弱，要么根本不表达；转位作用已被排除，但这种Kn1表达改变的原因尚不清楚。我们的工作假设是，Kn1突变体使得一种通常不在叶原基细胞中产生的产物得以表达。我们认为这种产物干扰了侧脉附近细胞早期的细胞类型定向。因此，在更为成熟的叶片中存在相对未定向的细胞，这些细胞可能意外分裂形成扭结，或者诱导出小块叶舌。