Department of Integrative Biological Sciences & BK21 FOUR Educational Research Group for Age-associated Disorder Control Technology, Chosun University, Gwangju, 61452, Republic of Korea.
Department of Integrative Biological Sciences & BK21 FOUR Educational Research Group for Age-associated Disorder Control Technology, Chosun University, Gwangju, 61452, Republic of Korea.
Biochem Biophys Res Commun. 2022 Nov 12;629:106-111. doi: 10.1016/j.bbrc.2022.09.024. Epub 2022 Sep 10.
Phosphatidylinositol 3-Kinase (PI3K) is a key regulator of cell motility during chemotaxis and plays an important role in relaying and amplifying the shallow gradient of chemoattractant signals to ultimately mediate rearrangements of the actin cytoskeleton. To determine whether PI3K plays a similar role in electrotaxis as in chemotaxis, we examined directional cell migration in response to an electric field (EF) and unexpectedly found that the role of PI3K in regulating cell motility differs depending on the state of Dictyostelium cells. Contrary to chemotaxis experiments using aggregation-competent cells, in the cell migration assay, we used a recently developed method for electrotaxis using 3-h starved cells. Wild-type cells starved for 3 h showed increased motility in the presence of LY294002, a PI3K inhibitor, whereas aggregation-competent cells showed slightly decreased motility, indicating the effect of LY294002 on cell motility differ depending on the state of the cells. Consistent with these results, pi3k null cells in the vegetative state exhibited increased motility similar to that in the presence of LY294002, compared to wild-type cells. These findings were confirmed through random migration experiments. These results suggest that PI3Ks play a suppressive role in regulating cell motility of vegetative Dictyostelium cells and that the suppressive effect is reversed on inhibition or lack of PI3Ks, leading to high motility.
磷脂酰肌醇 3-激酶 (PI3K) 是趋化作用过程中细胞运动的关键调节剂，在传递和放大趋化因子信号的浅梯度方面发挥重要作用，最终介导肌动蛋白细胞骨架的重排。为了确定 PI3K 在电趋性中是否发挥与趋化性类似的作用，我们研究了细胞对电场 (EF) 的定向迁移，出人意料地发现 PI3K 在调节细胞运动中的作用取决于盘基网柄菌细胞的状态。与使用聚集能力细胞的趋化性实验相反，在细胞迁移实验中，我们使用了最近开发的使用 3 小时饥饿细胞进行电趋性的方法。在存在 PI3K 抑制剂 LY294002 的情况下，饥饿 3 小时的野生型细胞表现出增强的运动性，而聚集能力细胞表现出略低的运动性，表明 LY294002 对细胞运动性的影响取决于细胞的状态。与这些结果一致，与野生型细胞相比，营养态的 pi3k 缺失细胞表现出与 LY294002 存在时相似的增强运动性。这些发现通过随机迁移实验得到了证实。这些结果表明，PI3Ks 在调节营养态盘基网柄菌细胞的细胞运动中起抑制作用，并且抑制作用在抑制或缺乏 PI3Ks 时被逆转，导致高运动性。
