Pereyra E, Ingerfeld M, Anderson N, Jackson S L, Moreno S
Departamento de Química Biológica, Facultad de Ciencias Exactas y Naturales, Universidad de Buenos Aires, Buenos Aires, Argentina.
Protoplasma. 2006 Sep;228(4):189-99. doi: 10.1007/s00709-006-0184-0. Epub 2006 Sep 20.
A comparative analysis of the effect of two compounds, dibutyryl-cyclic-AMP (dbcAMP) and latrunculin B, on the morphology and ultrastructure of the dimorphic fungus Mucor rouxii under aerobic growth conditions is presented. dbcAMP acts through the sustained activation of protein kinase A, and latrunculin B through the disruption of the actin cytoskeleton. Upon addition of these compounds to the growth medium at any stage of the germination process, cells lost polarised growth and switched to isodiametric growth. The effect was reversible. The morphologies, visualised by light microscopy or scanning electron microscopy (SEM), were alike. A switch from a rough to a smooth surface was observed by SEM when cells were repolarised by removal of the added compound. Ultrastructural changes under both conditions, as observed by transmission electron microscopy, were similar, the main feature being the enlargement of the cell wall, with irregular depositions, and detachment from the cell membrane. dbcAMP-treated cells showed a decrease in the number of glycogen granules compared with control and latrunculin B-treated cells. F-actin staining with fluorescein isothiocyanate-phalloidin showed that both dbcAMP- and latrunculin B-treated cells displayed a much lower fluorescence than control cells, with only a few pale plaques. The results suggest that the sustained activation of protein kinase A, which impairs polarised growth, might exert its effect through a modification of actin cytoskeleton organisation, very probably also involving an integrinlike pathway, as judged by the cell wall detachment and loss of cell adhesiveness of the dbcAMP-treated isodiametric cells.
本文对两种化合物——二丁酰环磷腺苷(dbcAMP)和拉春库林B,在有氧生长条件下对双态真菌鲁氏毛霉的形态和超微结构的影响进行了比较分析。dbcAMP通过持续激活蛋白激酶A发挥作用,而拉春库林B则通过破坏肌动蛋白细胞骨架发挥作用。在萌发过程的任何阶段,将这些化合物添加到生长培养基中后,细胞失去极性生长并转变为等径生长。这种影响是可逆的。通过光学显微镜或扫描电子显微镜(SEM)观察到的形态相似。当通过去除添加的化合物使细胞重新极化时,SEM观察到细胞表面从粗糙变为光滑。通过透射电子显微镜观察,在两种条件下的超微结构变化相似,主要特征是细胞壁增大,有不规则沉积物,并且与细胞膜分离。与对照和拉春库林B处理的细胞相比,dbcAMP处理的细胞中糖原颗粒数量减少。用异硫氰酸荧光素 - 鬼笔环肽进行F - 肌动蛋白染色显示,dbcAMP和拉春库林B处理的细胞荧光均比对照细胞低得多,只有少数淡色斑块。结果表明,持续激活的蛋白激酶A损害极性生长,可能通过改变肌动蛋白细胞骨架组织发挥作用,很可能还涉及一种类整合素途径,这从dbcAMP处理的等径细胞的细胞壁分离和细胞粘附丧失可以判断出来。