Xeroderma Pigmentosum D (XPD, also known as ERCC2) is a multi-functional protein involved in transcription, DNA repair and chromosome segregation. In Drosophila, Xpd interacts with Crumbs (Crb) and Galla to regulate mitosis during embryogenesis. It is unknown how these proteins are linked to mitosis. Here, we show that Crb, Galla-2 and Xpd regulate nuclear division in the syncytial embryo by interacting with Klp61F, the Drosophila mitotic Kinesin-5 associated with bipolar spindles. Crb, Galla-2 and Xpd physically interact with Klp61F and colocalize to mitotic spindles. Knockdown of any of these proteins results in similar mitotic defects. These phenotypes are restored by overexpression of Klp61F, suggesting that Klp61F is a major effector. Mitotic defects of galla-2 RNAi are suppressed by Xpd overexpression but not vice versa. Depletion of Crb, Galla-2 or Xpd results in a reduction of Klp61F levels. Reducing proteasome function restores Klp61F levels and suppresses mitotic defects caused by knockdown of Crb, Galla-2 or Xpd. Furthermore, eye growth is regulated by Xpd and Klp61F. Hence, we propose that Crb, Galla-2 and Xpd interact to maintain the level of Klp61F during mitosis and organ growth.

色素干皮病 D（XPD，也称为 ERCC2）是一种参与转录、DNA 修复和染色体分离的多功能蛋白。在果蝇中，Xpd 与 Crumbs (Crb) 和 Galla 相互作用，在胚胎发生过程中调节有丝分裂。目前尚不清楚这些蛋白质如何与有丝分裂相关。在这里，我们发现 Crb、Galla-2 和 Xpd 通过与 Klp61F（与双极纺锤体相关的果蝇有丝分裂驱动蛋白 5 ）相互作用来调节合胞体胚胎中的核分裂。Crb、Galla-2 和 Xpd 与 Klp61F 发生物理相互作用并共定位于有丝分裂纺锤体。任何这些蛋白质的敲低都会导致类似的有丝分裂缺陷。这些表型通过 Klp61F 的过度表达而恢复，表明 Klp61F 是主要效应子。Xpd 过表达可抑制galla-2 RNAi的有丝分裂缺陷，但反之则不然。Crb、Galla-2 或 Xpd 的消耗会导致 Klp61F 水平降低。降低蛋白酶体功能可恢复 Klp61F 水平并抑制因 Crb、Galla-2 或 Xpd 敲低而引起的有丝分裂缺陷。此外，眼睛的生长受 Xpd 和 Klp61F 的调节。因此，我们建议 Crb、Galla-2 和 Xpd 相互作用以在有丝分裂和器官生长过程中维持 Klp61F 的水平。