Elucidating the role of the AP2 endocytic adaptor complex on C.albicans virulence.

我们已经在白色念珠菌中删除了AP2内吞接头复合体的一个重要亚基，并观察到极化生长中的显著缺陷。如前所述，apm4缺失突变体在诱导条件下不能形成细长的丝状细胞，而是生长宽大和畸形的菌丝。突变体在液体相的内吞作用中只受到轻微的损害，这使我们假设AP2在特定货物的内吞作用中发挥作用，这对极化生长是重要的。最近已经清楚的是，内吞和分泌的平衡对于丝状真菌中的高度极化生长至关重要，然而许多关键角色仍不清楚(Schultzhaus和Shaw，2017)。这种极化生长是细胞生物学的一个关键方面，也是白念珠菌毒力的核心(Mayer等人，2013年)。因此，阐明AP2内吞接头复合体在白念珠菌菌丝生长和毒力中的作用具有重要意义。

We have deleted an essential subunit of the AP2 endocytic adaptor complex in Candida albicans, and observed marked defects in polarised growth. As shown previously, the apm4 deletion mutant is unable to form long, thin filamentous cells under inducing conditions, instead growing wide and misshapen hyphae. The mutant is only slightly impaired in fluid phase endocytosis, leading us to hypothesise that AP2 plays a role in the endocytosis of specific cargoes which are important to polarised growth. It has recently become clear that a balance of endocytosis and secretion is essential for the highly polarised growth seen in filamentous fungi, however many of the key players remain unknown (Schultzhaus and Shaw, 2017). This polarised growth is a key aspect of cell biology, and is also central to Candida albicans virulence (Mayer et al., 2013). Therefore, elucidating the role of the AP2 endocytic adaptor complex in hyphal growth and virulence of Candida albicans is of great importance.