Selden S C, Pollard T D
J Biol Chem. 1983 Jun 10;258(11):7064-71.
We have determined the absolute phosphate content of microtubule-associated proteins (MAPs) and established that phosphorylation inhibits the actin filament cross-linking activity of MAPs and both of the major MAP components, MAP-2 and tau. Similar results were obtained with actin from rabbit muscle, hog brain, and Acanthamoeba castellanii. We used the endogenous phosphatases and kinases in hog brain microtubule protein to modulate MAP phosphate level before isolating heat-stable MAPs. MAPs isolated directly from twice-cycled microtubule protein contain 7.1 +/- 0.1 (S.E.) mol of phosphate/300,000 g protein. After incubating microtubule protein without ATP, MAPs, had 4.9 +/- 0.6 phosphates. After incubating microtubule protein with 1 mM ATP and 5 microM cAMP in 2 mM EGTA, MAPs had 8.6 +/- 0.5 phosphates but there was also exchange of three more [32P]phosphates from gamma-labeled ATP for preexisting MAP phosphate. Incubation of microtubule protein with ATP and cAMP in 5 mM CaCl2 resulted in exchange but no net addition of phosphate to MAPs. We fractionated the MAP preparations by gel filtration and obtained MAP-2 with 4.3 to 7.5 and tau with 1.5 to 2.2 mol of phosphate/mol of protein depending on how we treated the microtubule protein prior to MAP isolation. The actin filament cross-linking activity of whole MAPs, MAP-2, and tau depended on the MAP-phosphate content. In all cases, phosphorylation of MAPs inhibited actin filament cross-linking activity. The concentration of high phosphate MAPs required to form a high viscosity solution with actin filaments was 2 to 4 times more than that of low phosphate. MAPs. During incubation of microtubule protein with [gamma-32P]ATP, only MAP peptides are labeled. Treatment of these MAPs with either acid or alkaline phosphatase removes phosphate mainly from MAP-2, with an increase in actin filament cross-linking activity. Thus, both MAP phosphorylation and the effect of phosphorylation on actin cross-linking activity of MAPs are reversible.
我们测定了微管相关蛋白(MAPs)的绝对磷酸含量,并证实磷酸化会抑制MAPs以及两种主要MAP成分(MAP-2和tau)的肌动蛋白丝交联活性。用来自兔肌肉、猪脑和卡氏棘阿米巴的肌动蛋白也得到了类似结果。在分离热稳定MAPs之前,我们利用猪脑微管蛋白中的内源性磷酸酶和激酶来调节MAP的磷酸水平。直接从经过两次循环的微管蛋白中分离得到的MAPs含有7.1±0.1(标准误)摩尔磷酸/300,000克蛋白质。在无ATP条件下孵育微管蛋白后,MAPs含有4.9±0.6个磷酸基团。在2 mM乙二醇双乙醚四乙酸(EGTA)存在下,将微管蛋白与1 mM ATP和5 μM环磷酸腺苷(cAMP)一起孵育后,MAPs含有8.6±0.5个磷酸基团,但同时还有另外三个来自γ标记ATP的[32P]磷酸基团与MAPs原有的磷酸基团发生交换。在5 mM氯化钙(CaCl2)存在下,将微管蛋白与ATP和cAMP一起孵育会导致交换,但不会使MAPs的磷酸基团净增加。我们通过凝胶过滤对MAP制剂进行分级分离,根据在分离MAPs之前对微管蛋白的处理方式不同,得到的MAP-2含有4.3至7.5摩尔磷酸/摩尔蛋白质,tau含有1.5至2.2摩尔磷酸/摩尔蛋白质。完整的MAPs、MAP-2和tau的肌动蛋白丝交联活性取决于MAP的磷酸含量。在所有情况下,MAPs的磷酸化都会抑制肌动蛋白丝交联活性。与肌动蛋白丝形成高粘度溶液所需的高磷酸化MAPs的浓度是低磷酸化MAPs的2至4倍。在微管蛋白与[γ-32P]ATP孵育期间,只有MAP肽段被标记。用酸性或碱性磷酸酶处理这些MAPs会使磷酸基团主要从MAP-2上移除,同时肌动蛋白丝交联活性增加。因此,MAP的磷酸化以及磷酸化对MAPs肌动蛋白交联活性的影响都是可逆的。