BackgroundIn Drosophila, the development of the fly eye involves the activity of several, interconnected pathways that first define the presumptive eye field within the eye anlagen, followed by establishment of the dorso-ventral boundary, and the regulation of growth and apoptosis. In Lobe (L) mutant flies, parts of the eye or even the complete eye are absent because the eye field has not been properly defined. Manifold genetic interactions indicate that L influences the activity of several signalling pathways, resulting in a conversion of eye tissue into epidermis, and in the induction of apoptosis. As information on the molecular nature of the L mutation is lacking, the underlying molecular mechanisms are still an enigma.ResultsWe have identified Protein Kinase D (PKD) as a strong modifier of the L mutant phenotype. PKD belongs to the PKC/CAMK class of Ser/Thr kinases that have been involved in diverse cellular processes including stress resistance and growth. Despite the many roles of PKD, Drosophila PKD null mutants are without apparent phenotype apart from sensitivity to oxidative stress. Here we report an involvement of PKD in eye development in the sensitized genetic background of Lobe. Absence of PKD strongly enhanced the dominant eye defects of heterozygous L2 flies, and decreased their viability. Moreover, eye-specific overexpression of an activated isoform of PKD considerably ameliorated the dominant L2 phenotype. This genetic interaction was not allele specific but similarly seen with three additional, weaker L alleles (L1, L5, LG), demonstrating its specificity.ConclusionsWe propose that PKD-mediated phosphorylation is involved in underlying processes causing the L phenotype, i.e. in the regulation of growth, the epidermal transformation of eye tissue and apoptosis, respectively.

中文翻译：

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黑腹果蝇眼睛发育过程中蛋白激酶D与叶突变体的遗传相互作用

背景在果蝇中，蝇眼的发育涉及多个相互关联的途径的活动，这些途径首先定义了眼原基内的假定眼场，然后是背腹边界的建立，以及生长和细胞凋亡的调节。在 Lobe (L) 突变果蝇中，部分眼睛甚至整个眼睛都不存在，因为没有正确定义眼场。多种遗传相互作用表明 L 影响几种信号通路的活性，导致眼组织转化为表皮，并诱导细胞凋亡。由于缺乏关于 L 突变的分子性质的信息，其潜在的分子机制仍然是一个谜。结果我们已经确定蛋白激酶 D (PKD) 是 L 突变表型的强修饰剂。PKD 属于 PKC/CAMK 类的 Ser/Thr 激酶，这些激酶参与了多种细胞过程，包括抗逆性和生长。尽管 PKD 的许多作用，果蝇 PKD 无效突变体除了对氧化应激的敏感性外没有明显的表型。在这里，我们报告了 PKD 在叶的致敏遗传背景中参与眼睛发育。PKD 的缺乏强烈地增强了杂合 L2 果蝇的主要眼缺陷，并降低了它们的生存能力。此外，激活的 PKD 同种型的眼睛特异性过表达显着改善了主要的 L2 表型。这种遗传相互作用不是等位基因特异性的，但与另外三个较弱的 L 等位基因（L1、L5、LG）类似，证明了它的特异性。