Sealey-Cardona Marco, Schmidt Katy, Demmel Lars, Hirschmugl Tatjana, Gesell Tanja, Dong Gang, Warren Graham
Max F. Perutz Laboratories, University of Vienna and Medical University of Vienna, Dr. Bohr-Gasse 9/3, 1030, Vienna, Austria.
Traffic. 2014 Jun;15(6):613-29. doi: 10.1111/tra.12170. Epub 2014 Apr 4.
The Sec16 homologue in Trypanosoma brucei has been identified and characterized. TbSec16 colocalizes with COPII components at the single endoplasmic reticulum exit site (ERES), which is next to the single Golgi stack in the insect (procyclic) form of this organism. Depletion of TbSec16 reduces the size of the ERES and the Golgi, and slows growth and transport of a secretory marker to the cell surface; conversely, overexpression of TbSec16 increases the size of the ERES and Golgi but has no effect on growth or secretion. Together these data suggest that TbSec16 regulates the size of the ERES and Golgi and this size is set for optimal growth of the organism.
布氏锥虫中的Sec16同源物已被鉴定和表征。TbSec16与COPII组分共定位于单个内质网出口位点（ERES），该位点在这种生物体的昆虫（前循环）形式中紧邻单个高尔基体堆栈。TbSec16的缺失会减小ERES和高尔基体的大小，并减缓分泌标记物向细胞表面的生长和运输；相反，TbSec16的过表达会增加ERES和高尔基体的大小，但对生长或分泌没有影响。这些数据共同表明，TbSec16调节ERES和高尔基体的大小，并且这个大小是为生物体的最佳生长而设定的。
