Ttk69-dependent repression of lozenge prevents the ectopic development of R7 cells in the Drosophila larval eye disc.
Ttk69-dependent repression of lozenge prevents the ectopic development of R7 cells in the Drosophila larval eye disc.
复制标题
TTK69依赖于lozenge的抑制阻止了果蝇幼虫眼盘R7细胞的异位发育。
DOI：
10.1186/1471-213x-9-64
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发表时间：
2009-12-09
影响因子：
--
通讯作者：
Batterham P
中科院分区：
文献类型：
--
作者：
Siddall NA;Hime GR;Pollock JA;Batterham P
在果蝇眼睛的发育过程中，特定的细胞类型从最初的等能的未定型前体细胞群中分化出来。菱形（lozenge，lz）基因是Runt家族转录调控因子的一员，通过调控多种命运特异性转录因子的表达，在介导这一过程中起着关键作用。然而，lz的调节和不同细胞类型中lz表达水平的控制还没有完全理解。在这里，我们展示了Tramtrack 69（Ttk 69）的关键转录抑制因子和神经元命运规范的抑制剂，和LZ，主图案化基因的细胞后的果蝇眼盘的形态发生沟之间的遗传相互作用。Ttk 69表达的丧失导致三龄眼盘中异位R7细胞的发育，这些细胞的发育依赖于Lz。使用二元UAS Gal 4系统，我们发现Ttk 69的过表达导致Lz依赖性分化细胞的丢失，以及发育中的眼睛中Lz表达的下调。lz依赖性细胞的损失可以通过经由GMR-lz转基因过表达lz来挽救。我们提供了额外的数据表明，在眼睛发育中Ttk 69上游发挥作用的因子以Ttk 69依赖的方式调节lz。我们的研究结果使我们得出结论，Ttk 69可以直接或间接抑制lz基因的表达，以防止R7前体细胞在发育中的果蝇眼睛的过早发育。因此，我们定义了一个机制，严格的监管控制的主预图案化基因，lz，在早期果蝇眼睛的发展，并提供洞察力如何差异水平的lz表达可以实现特定的细胞命运的结果。
During the development of the Drosophila eye, specific cell types differentiate from an initially equipotent group of uncommitted precursor cells. The lozenge (lz) gene, which is a member of the Runt family of transcriptional regulators, plays a pivotal role in mediating this process through regulating the expression of several fate-specifying transcription factors. However, the regulation of lz, and the control of lz expression levels in different cell types is not fully understood. Here, we show a genetic interaction between Tramtrack69 (Ttk69) a key transcriptional repressor and an inhibitor of neuronal fate specification, and lz, the master patterning gene of cells posterior to the morphogenetic furrow in the Drosophila eye disc. Loss of Ttk69 expression causes the development of ectopic R7 cells in the third instar eye disc, with these cells being dependent upon Lz for their development. Using the binary UAS Gal4 system, we show that overexpression of Ttk69 causes the loss of lz-dependent differentiating cells, and a down-regulation of Lz expression in the developing eye. The loss of lz-dependent cells can be rescued by overexpressing lz via a GMR-lz transgene. We provide additional data showing that factors functioning upstream of Ttk69 in eye development regulate lz in a Ttk69-dependent manner. Our results lead us to conclude that Ttk69 can either directly or indirectly repress lz gene expression to prevent the premature development of R7 precursor cells in the developing eye of Drosophila. We therefore define a mechanism for the tight regulatory control of the master pre-patterning gene, lz, in early Drosophila eye development and provide insight into how differential levels of lz expression can be achieved to effect specific cell fate outcomes.