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151.
Archeospores of Porphyra pulchella Ackland, J. A. West et Zuccarello (Rhodophyta) display amoeboid and gliding motility. Time‐lapse videomicroscopy revealed that amoeboid cells extend and retract pseudopodia as they translocate through the media. We investigated the involvement of actin and myosin in generating the force for amoeboid motility using immunofluorescence, time‐lapse videomicroscopy, and cytoskeletal inhibitors. Actin filaments were seen as short and long rodlike bundles around the periphery of spores. The actin inhibitors cytochalasin D (CD) and latrunculin B (Lat B), and the myosin inhibitor butanedione monoxime (BDM) disrupted the actin filament network and reversibly inhibited pseudopodial activity, resulting in the rounding and immobilization of spores. It was uncertain whether forward translocation of archeospores resumed following drug removal. These results demonstrate that actin and myosin have a role in generating force for pseudopodial activity. This is the first report of cytoskeletal involvement in red algal cell movement. The involvement of actin and myosin in forward translocation of amoeboid archeospores can only be speculated upon. 相似文献
152.
Cloning of the cDNA and nucleotide sequence of a skeletal muscle protease from myopathic hamsters 总被引:2,自引:0,他引:2
Holt John C. Hatchert Victor B. Caulfield James B. Norton Paul Umeda Patrick K. Melendez J. Andres Martino Leon Mudzinsky Stanley P. Blumenstock Frank Slayter Henry S. Margossian Sarkis S. 《Molecular and cellular biochemistry》1998,181(1-2):125-135
A neutral protease with an estimated Mr of about 26 kD and responsible for cleavage of myosin LC2 was isolated from hamster skeletal muscle. Complementary DNAs were generated by RT-PCR using total hamster muscle RNA and degenerate oligonucleotide primers based on the sequences of two internal peptides. The nucleotide sequences of the resultant cDNAs were subsequently determined and the complete amino acid sequence of the protease deduced. Although the hamster protein shared 63-85% identity in nucleotide and amino acid sequences with rat and mouse mast cell proteases, it had a higher degree of specificity for myosin LC2 than mast cell proteases which also digested myosin LC1 and myosin heavy chains. As a result, the hamster protease was designated mekratin because of its unique enzymatic specificities to distinguish it from other mast cell proteases. A polyclonal antibody was raised specific to the hamster muscle and human cardiac muscle mekratins without apparent cross-reaction with rat mast cell proteases. We have earlier demonstrated the presence in excess of a neutral protease that specifically cleaves LC2 in human hearts obtained at end stage idiopathic dilated cardiomyopathy (IDC). Western analyses revealed that heart tissue from patients with IDC contained 5-10 fold more mekratin than control samples. Furthermore, the level of the protease in human IDC tissues was similar to that seen in myopathic hamster skeletal muscle. No bands were recognized by the antibody when IDC myofibrils were probed due to the removal of soluble proteins during sample preparation. Thus, these results strongly suggest that the anti-mekratin antibody will provide positive identification of IDC in many cases and diagnosis by exclusion may be replaced. 相似文献
153.
Taichi Ikedo Manabu Minami Hiroharu Kataoka Kosuke Hayashi Manabu Nagata Risako Fujikawa Fumiyoshi Yamazaki Mitsutoshi Setou Masayuki Yokode Susumu Miyamoto 《Biochemical and biophysical research communications》2018,495(1):332-338
Object
The wall thickness of intracranial aneurysms (IAs) is heterogeneous. Although thinning of the IA wall is thought to contribute to IA rupture, the underlying mechanism remains poorly understood. Recently, imaging mass spectroscopy (IMS) has been used to reveal the distribution of phospholipids in vascular diseases. To investigate the feature of phospholipid composition of IA walls, we conducted IMS in a rat model of experimentally induced IA.Material and methods
IAs were surgically induced in 7-week-old male rats and analyzed by IMS in negative-ion mode.Results
A molecule at m/z 885.5 was more abundant in the thickened wall than in the thinned wall (P = 0.03). Multiple-stage mass spectroscopy revealed the molecule to be phosphatidylinositol containing stearic acid and arachidonic acid (PI 18:0/20:4). Immunohistochemistry indicated that vascular smooth muscle cells (SMCs) in the thickened wall had dedifferentiated phenotypes. To investigate the relationship between accumulation of PI (18:0/20:4) and phenotypic changes in SMCs, we subjected primary mouse aortic SMCs to liquid chromatography–tandem mass spectrometry. Notably, dedifferentiated SMCs had 1.3-fold more PI (18:0/20:4) than partly differentiated SMCs.Conclusions
Our study demonstrated the heterogeneity in phospholipid composition of the aneurysmal walls using experimentally induced IAs. PI (18:0/20:4) accumulated at high levels in the thickened aneurysmal wall where synthetic dedifferentiated SMCs exist, suggesting that this phospholipid may be involved in the phenotypic switching of medial SMCs in the IA wall. 相似文献154.
Primary skeletal muscle cells cultured on gelatin bead microcarriers develop structural and biochemical features characteristic of adult skeletal muscle 下载免费PDF全文
155.
Jonathan Walklate Carlos Vera Marieke J. Bloemink Michael A. Geeves Leslie Leinwand 《The Journal of biological chemistry》2016,291(19):10318-10331
The embryonic myosin isoform is expressed during fetal development and rapidly down-regulated after birth. Freeman-Sheldon syndrome (FSS) is a disease associated with missense mutations in the motor domain of this myosin. It is the most severe form of distal arthrogryposis, leading to overcontraction of the hands, feet, and orofacial muscles and other joints of the body. Availability of human embryonic muscle tissue has been a limiting factor in investigating the properties of this isoform and its mutations. Using a recombinant expression system, we have studied homogeneous samples of human motors for the WT and three of the most common FSS mutants: R672H, R672C, and T178I. Our data suggest that the WT embryonic myosin motor is similar in contractile speed to the slow type I/β cardiac based on the rate constant for ADP release and ADP affinity for actin-myosin. All three FSS mutations show dramatic changes in kinetic properties, most notably the slowing of the apparent ATP hydrolysis step (reduced 5–9-fold), leading to a longer lived detached state and a slowed Vmax of the ATPase (2–35-fold), indicating a slower cycling time. These mutations therefore seriously disrupt myosin function. 相似文献
156.
rib and raw mutations prevent cells in a number of tissues from assuming specialized shapes, resulting in abnormal tubular epithelia
and failure of morphogenetic movements such as dorsal closure. Mutations of zip, which encodes the nonmuscle myosin heavy chain, suppress the phenotypes of rib and raw, suggesting that rib and raw are not directly required for myosin function. Abnormal formation of the actin cytoskeletal structures underlying embryonic
cuticular hairs suggests possible roles for rib and raw in organizing the actin cytoskeleton. The actin prehair structures are absent in rib mutants and abnormally shaped in raw mutants, indicating that the two genes have different functions required for organizing the actin cytoskeleton.
Received: 4 December 1998 / Accepted: 26 January 1999 相似文献
157.
运动对高血压性肥大心脏心肌肌球蛋白重链基因表达的影响 总被引:7,自引:0,他引:7
研究运动逆转高血压肥大心脏心肌肌球蛋白重链(myosin heavy chain ,MHC)异型改变的分子机制。方法:采用Northern 分子杂交方法对自发性高血压大鼠(spontaneously hypertensive rats,SHR) 游泳运动10 周后心肌MHC基因表达进行比较研究。结果:游泳SHR收缩压和舒张压分别比安静SHR 降低22 % 和25% (P< 0.01) 。左心室重/体重(LVW/BW)比值两组间无明显差异(P> 0.05)。游泳SHR 心肌αMHCmRNA表达比安静SHR增强17% ,βMHCmRNA 表达降低26 % ,α/βMHC基因表达比值提高59 % 。结论:运动逆转高血压肥大心脏心肌MHC同型异构体转变的调控机制可发生在基因转录水平上 相似文献
158.
159.
NELSON A. MEDEIROS THOMAS S. REESE HOWARD JAFFE JOSEPH A. DEGIORGIS ELAINE L. BEARER 《Cell biology international》1998,22(2):161-173
The squid giant axon provides an excellent model system for the study of actin-based organelle transport likely to be mediated by myosins, but the identification of these motors has proven to be difficult. Here the authors purified and obtained primary peptide sequence of squid muscle myosin as a first step in a strategy designed to identify myosins in the squid nervous system. Limited digestion yielded fourteen peptides derived from the muscle myosin which possess high amino acid sequence identities to myosin II from scallop (60–95%) and chick pectoralis muscle (31–83%). Antibodies generated to this purified muscle myosin were used to isolate a potential myosin from squid optic lobe which yielded 11 peptide fragments. Sequences from six of these fragments identified this protein as a myosin II. The other five sequences matched myosin II (50–60%, identities), and some also matched unconventional myosins (33–50%). A single band that has a molecular weight similar to the myosin purified from optic lobe copurifies with axoplasmic organelles, and, like the optic lobe myosin, this band is also recognized by the antibodies raised against squid muscle myosin II. Hence, this strategy provides an approach to the identification of a myosin associated with motile axoplasmic organelles. 相似文献
160.
Yumura S Ueda M Sako Y Kitanishi-Yumura T Yanagida T 《Traffic (Copenhagen, Denmark)》2008,9(12):2089-2099
Total internal reflection fluorescence microscopy revealed how individual bipolar myosin II filaments accumulate at the equatorial region in dividing Dictyostelium cells. Direct observation of individual filaments in live cells provided us with much convincing information. Myosin II filaments accumulated at the equatorial region by at least two independent mechanisms: (i) cortical flow, which is driven by myosin II motor activities and (ii) de novo association to the equatorial cortex. These two mechanisms were mutually redundant. At the same time, myosin II filaments underwent rapid turnover, repeating their association and dissociation with the actin cortex. Examination of the lifetime of mutant myosin filaments in the cortex revealed that the turnover mainly depended on heavy chain phosphorylation and that myosin motor activity accelerated the turnover. Double mutant myosin II deficient in both motor and phosphorylation still accumulated at the equatorial region, although they displayed no cortical flow and considerably slow turnover. Under this condition, the filaments stayed for a significantly longer time at the equatorial region than at the polar regions, indicating that there are still other mechanisms for myosin II accumulation such as binding partners or stabilizing activity of filaments in the equatorial cortex. 相似文献