Krymsky M A, Kudryashov D S, Shirinsky V P, Lukas T J, Watterson D M, Vorotnikov A V
Laboratory of Cell Motility, Institute of Experimental Cardiology, Cardiology Research Centre, Moscow, Russia.
J Muscle Res Cell Motil. 2001;22(5):425-37. doi: 10.1023/a:1014503604270.
KRP (telokin), an independently expressed C-terminal myosin-binding domain of smooth muscle myosin light chain kinase (MLCK), has been reported to have two related functions. First, KRP stabilizes myosin filaments (Shirinsky et al., 1993, J. Biol. Chem. 268, 16578-16583) in the presence of ATP. Secondly, KRP can modulate the level of myosin light chain phosphorylation. In this latter role, multiple mechanisms have been suggested. One hypothesis is that light chain phosphorylation is diminished by the direct competition of KRP and MLCK for myosin, resulting in a loss of contraction. Alternatively, KRP, through an unidentified mechanism, accelerates myosin light chain dephosphorylation in a manner possibly enhanced by KRP phosphorylation. Here, we demonstrate that KRP is a major phosphoprotein in smooth muscle, and use a comparative approach to investigate how its phosphorylation correlates with sustained contraction and forskolin-induced relaxation. Forskolin relaxation of precontracted artery strips caused little increase in KRP phosphorylation, while treatment with phorbol ester increased the level of KRP phosphorylation without a subsequent change in contractility. Although phorbol ester does not induce contraction of phasic tissues, the level of KRP phosphorylation is increased. Phosphopeptide maps of KRP from both tissues revealed multiple sites of phosphorylation within the N-terminal region of KRP. Phosphopeptide maps of KRP from gizzard were more complex than those for KRP from artery consistent with heterogeneity at the amino terminus and/or additional sites. We discovered through analysis of KRP phosphorylation in vitro that Ser12, Ser15 and Ser15 are phosphorylated by cAMP-dependent protein kinase, mitogen-activated protein (MAP) kinase and glycogen synthase kinase 3 (GSK3), respectively. Phosphorylation by GSK3 was dependent upon prephosphorylation by MAP kinase. This appears to be the first report of conditional or hierarchical phosphorylation of KRP. Peptides consistent with such multiple phosphorylations were found on the in vivo phosphopeptide maps of avian KRP. Collectively, the available data indicate that there is a complex relationship between the in vivo phosphorylation states of KRP and its effects on relaxation in smooth muscle.
KRP(telokin)是平滑肌肌球蛋白轻链激酶(MLCK)独立表达的C末端肌球蛋白结合结构域,据报道具有两种相关功能。首先,KRP在ATP存在的情况下可稳定肌球蛋白丝(Shirinsky等人,1993年,《生物化学杂志》268卷,16578 - 16583页)。其次,KRP可调节肌球蛋白轻链磷酸化水平。关于后一种作用,已提出多种机制。一种假说是,KRP和MLCK对肌球蛋白的直接竞争减少了轻链磷酸化,导致收缩丧失。或者,KRP通过一种不明机制,以可能因KRP磷酸化而增强的方式加速肌球蛋白轻链去磷酸化。在此,我们证明KRP是平滑肌中的主要磷蛋白,并采用比较方法研究其磷酸化与持续收缩和福斯可林诱导的舒张如何相关。预收缩动脉条带经福斯可林舒张后,KRP磷酸化几乎没有增加,而用佛波酯处理可增加KRP磷酸化水平,且随后收缩性无变化。尽管佛波酯不诱导相性组织收缩,但KRP磷酸化水平增加。来自这两种组织的KRP的磷酸肽图谱显示在KRP的N末端区域内有多个磷酸化位点。来自砂囊的KRP的磷酸肽图谱比来自动脉的KRP的磷酸肽图谱更复杂,这与氨基末端的异质性和/或其他位点一致。我们通过体外分析KRP磷酸化发现,Ser12、Ser15和Ser15分别被cAMP依赖性蛋白激酶、丝裂原活化蛋白(MAP)激酶和糖原合酶激酶3(GSK3)磷酸化。GSK3的磷酸化依赖于MAP激酶的预磷酸化。这似乎是关于KRP的条件性或分级磷酸化的首次报道。在禽类KRP的体内磷酸肽图谱上发现了与这种多重磷酸化一致的肽段。总体而言,现有数据表明KRP的体内磷酸化状态与其对平滑肌舒张的影响之间存在复杂关系。