Epidermal tendon cells require Broad Complex function for correct attachment of the indirect flight muscles in Drosophila melanogaster.
Epidermal tendon cells require Broad Complex function for correct attachment of the indirect flight muscles in Drosophila melanogaster.
复制标题
DOI：
--
复制
发表时间：
1999-11
影响因子：
4
通讯作者：
D. Sandstrom;L. Restifo
中科院分区：
文献类型：
--
作者：
D. Sandstrom;L. Restifo
果蝇广泛复合体是蜕皮激素级联反应中的一个初级反应基因，编码一个变态所必需的锌指转录因子家族。广泛的复杂突变的rbp互补组破坏附着的背腹侧间接飞行肌肉在蛹的发展。我们以前证明，同种型BRC-Z1介导rbp（+）的肌肉附着功能，并在发育中的肌纤维及其表皮附着部位表达。我们现在报告两个互补的研究，以确定在背腹间接飞行肌的肌腱连接成熟过程中rbp（+）的细胞位点和作用方式。首先，使用父系丢失方法产生的遗传镶嵌显示，肌肉附着表型主要由背侧表皮的基因型决定，肌纤维和腹侧表皮施加很少或没有影响。当背表皮突变，绝大多数肌肉脱落或选择异位附着位点，无论肌肉基因型。相反，野生型背表皮可以支持突变体肌肉的附着。其次，超微结构分析证实并扩展了这些结果，揭示了缺陷和延迟分化的rbp突变的表皮肌腱细胞在背附着网站。肌腱细胞突起，表皮和肌肉之间的应力轴承联系，数量减少，并表现出延迟出现的微管束。相比之下，突变体的肌肉和腹表皮类似于野生型。总之，BRC-Z1在背侧表皮中起作用以确保肌腱连接的分化。通过与胚胎肌肉附着所必需的细胞-细胞相互作用的类比，我们提出BRC-Z1调节表皮对来自发育中肌肉的信号的反应的一个或多个组分。
Drosophila Broad Complex, a primary response gene in the ecdysone cascade, encodes a family of zinc-finger transcription factors essential for metamorphosis. Broad Complex mutations of the rbp complementation group disrupt attachment of the dorsoventral indirect flight muscles during pupal development. We previously demonstrated that isoform BRC-Z1 mediates the muscle attachment function of rbp(+) and is expressed in both developing muscle fibers and their epidermal attachment sites. We now report two complementary studies to determine the cellular site and mode of action of rbp(+) during maturation of the myotendinous junctions of dorsoventral indirect flight muscles. First, genetic mosaics, produced using the paternal loss method, revealed that the muscle attachment phenotype is determined primarily by the genotype of the dorsal epidermis, with the muscle fiber and the ventral epidermis exerting little or no influence. When the dorsal epidermis was mutant, the vast majority of muscles detached or chose ectopic attachment sites, regardless of the muscle genotype. Conversely, wild-type dorsal epidermis could support attachment of mutant muscles. Second, ultrastructural analysis corroborated and extended these results, revealing defective and delayed differentiation of rbp mutant epidermal tendon cells in the dorsal attachment sites. Tendon cell processes, the stress-bearing links between the epidermis and muscle, were reduced in number and showed delayed appearance of microtubule bundles. In contrast, mutant muscle and ventral epidermis resembled the wild type. In conclusion, BRC-Z1 acts in the dorsal epidermis to ensure differentiation of the myotendinous junction. By analogy with the cell-cell interaction essential for embryonic muscle attachment, we propose that BRC-Z1 regulates one or more components of the epidermal response to a signal from the developing muscle.