Johnston L A, Prober D A, Edgar B A, Eisenman R N, Gallant P
Fred Hutchinson Cancer Research Center, Division of Basic Sciences, Seattle, Washington 98109, USA.
Cell. 1999 Sep 17;98(6):779-90. doi: 10.1016/s0092-8674(00)81512-3.
Transcription factors of the Myc proto-oncogene family promote cell division, but how they do this is poorly understood. Here we address the functions of Drosophila Myc (dMyc) during development. Using mosaic analysis in the fly wing, we show that loss of dMyc retards cellular growth (accumulation of cell mass) and reduces cell size, whereas dMyc overproduction increases growth rates and cell size. dMyc-induced growth promotes G1/S progression but fails to accelerate cell division because G2/M progression is independently controlled by Cdc25/String. We also show that the secreted signal Wingless patterns growth in the wing primordium by modulating dMyc expression. Our results indicate that dMyc links patterning signals to cell division by regulating primary targets involved in cellular growth and metabolism.
Myc原癌基因家族的转录因子可促进细胞分裂,但其具体机制尚不清楚。在此,我们研究了果蝇Myc(dMyc)在发育过程中的功能。利用果蝇翅膀的镶嵌分析,我们发现dMyc缺失会延缓细胞生长(细胞质量的积累)并减小细胞大小,而dMyc过量表达则会提高生长速率并增大细胞大小。dMyc诱导的生长促进G1/S期进程,但无法加速细胞分裂,因为G2/M期进程由Cdc25/String独立控制。我们还表明,分泌信号无翅蛋白通过调节dMyc表达来调控翅原基的生长模式。我们的结果表明,dMyc通过调节参与细胞生长和代谢的主要靶点,将模式信号与细胞分裂联系起来。