Intracellular Dynamics (intracellular + dynamics)

Distribution by Scientific Domains


Selected Abstracts


Intracellular dynamics of Smad-mediated TGF, signaling

JOURNAL OF CELLULAR PHYSIOLOGY, Issue 2 2003
Robert M. Greene
The transforming growth factor-, (TGF,) family represents a class of signaling molecules that plays a central role in morphogenesis, growth, and cell differentiation during normal embryonic development. Members of this growth factor family are particularly vital to development of the mammalian secondary palate where they regulate palate mesenchymal cell proliferation and extracellular matrix synthesis. Such regulation is particularly critical since perturbation of either cellular process results in a cleft of the palate. While the cellular and phenotypic effects of TGF, on embryonic craniofacial tissue have been extensively catalogued, the specific genes that function as downstream mediators of TGF, action in the embryo during palatal ontogenesis are poorly defined. Embryonic palatal tissue in vivo and murine embryonic palate mesenchymal (MEPM) cells in vitro secrete and respond to TGF,. In the current study, elements of the Smad component of the TGF, intracellular signaling system were identified and characterized in cells of the embryonic palate and functional activation of the Smad pathway by TGF,1, TGF,2, and TGF,3 was demonstrated. TGF,-initiated Smad signaling in cells of the embryonic palate was found to result in: (1) phosphorylation of Smad 2; (2) nuclear translocation of the Smads 2, 3, and 4 protein complex; (3) binding of Smads 3 and 4 to a consensus Smad binding element (SBE) oligonucleotide; (4) transactivation of transfected reporter constructs, containing TGF,-inducible Smad response elements; and (4) increased expression of gelatinases A and B (endogenous genes containing Smad response elements) whose expression is critical to matrix remodeling during palatal ontogenesis. Collectively, these data point to the presence of a functional Smad-mediated TGF, signaling system in cells of the developing murine palate. J. Cell. Physiol. 197: 261,271, 2003. © 2003 Wiley-Liss, Inc. [source]


Intracellular trafficking in neurones and glia of fibroblast growth factor-2, fibroblast growth factor receptor 1 and heparan sulphate proteoglycans in the injured adult rat cerebral cortex

JOURNAL OF NEUROCHEMISTRY, Issue 4 2006
W. E. Leadbeater
Abstract The potent gliogenic and neurotrophic fibroblast growth factor (FGF)-2 signals through a receptor complex comprising high-affinity FGF receptor (FGFR)1 with heparan sulphate proteoglycans (HSPGs) as co-receptors. We examined the intracellular dynamics of FGF-2, FGFR1 and the HSPGs syndecan-2 and -3, glypican-1 and -2, and perlecan in neurones and glia in and around adult rat cerebral wounds. In the intact cerebral cortex, FGF-2 and FGFR1 mRNA and protein were constitutively expressed in astrocytes and neurones respectively. FGF-2 protein was localized exclusively to astrocyte nuclei. After injury, expression of FGF-2 mRNA was up-regulated only in astrocytes, whereas FGFR1 mRNA expression was increased in both glia and neurones, a disparity indicating that FGF-2 may act as a paracrine and autocrine factor for neurones and glia respectively. FGF-2 protein localized to both cytoplasm and nuclei of injury-responsive neurones and glia. There was weak or no staining of HSPGs in the normal cerebral neuropil and glia nuclei, with a few immunopositive neurones. Specific HSPGs responded to injury by differentially co-localizing with trafficked intracellular FGF-2 and FGFR1. The spatiotemporal dynamics of FGF-2,FGFR1,HSPG complex formation implies a role for individual HSPGs in regulating FGF-2 storage, nuclear trafficking and cell-specific injury responses in CNS wounds. [source]


Three-photon microscopy shows that somatic release can be a quantitatively significant component of serotonergic neurotransmission in the mammalian brain

JOURNAL OF NEUROSCIENCE RESEARCH, Issue 15 2008
S.K. Kaushalya
Abstract Recent experiments on monoaminergic neurons have shown that neurotransmission can originate from somatic release. However, little is known about the quantity of monoamine available to be released through this extrasynaptic pathway or about the intracellular dynamics that mediate such release. Using three-photon microscopy, we directly imaged serotonin autofluorescence and investigated the total serotonin content, release competence, and release kinetics of somatic serotonergic vesicles in the dorsal raphe neurons of the rat. We found that the somata of primary cultured neurons contain a large number of serotonin-filled vesicles arranged in a perinuclear fashion. A similar distribution is also observed in fresh tissue slice preparations obtained from the rat dorsal raphe. We estimate that the soma of a cultured neuron on an average contains about 9 fmoles of serotonin in about 450 vesicles (or vesicle clusters) of ,370 nm average diameter. A substantial fraction (>30%) of this serotonin is released with a time scale of several minutes by K+ -induced depolarization or by para-chloroamphetamine treatment. The amount of releasable serotonin stored in the somatic vesicles is comparable to the total serotonin content of all the synaptic vesicles in a raphe neuron, indicating that somatic release can potentially play a major role in serotonergic neurotransmission in the mammalian brain. © 2008 Wiley-Liss, Inc. [source]


Tomato yellow leaf curl virus, the intracellular dynamics of a plant DNA virus

MOLECULAR PLANT PATHOLOGY, Issue 1 2003
Yedidya Gafni
SUMMARY Tomato yellow leaf curl virus is a geminivirus, transmitted by whitefly ( Bemisia tabaci ) and causing the most destructive disease of tomato throughout the Mediterranean region, the Middle East and the tropical regions of Africa and Central America. Affected plants produce either no fruits or a few small fruits. Since it is an ssDNA virus which replicates in the host cell nucleus, the molecular mechanisms involved in the viral nuclear import have been the focus of our studies in recent years and results as well as prospects will be discussed. Taxonomy:Tomato yellow leaf curl virus (TYLCV) is a ssDNA plant virus, a member of the family Geminiviridae , of the genus Begomovirus. Physical properties: ,TYLCV, like all members of Geminiviridae, has geminate (twinned) particles, 18,20 nm in diameter, 30 nm long, apparently consisting of two incomplete T = 1 icosahedra joined together in a structure with 22 pentameric capsomers and 110 identical protein subunits (Fig. 1). Figure 1. Particles of TYLCV. Electron micrograph of purified, negatively stained TYLCV particles. Bar = 100 nm. Disease symptoms: ,Symptoms become visible in tomato in approximately 2,3 weeks after infection (Fig. 2). Leaf symptoms include chlorotic margins, small leaves that are cupped, thick and rubbery. The majority (up to 90%) of flowers abscise after infection, and therefore few fruits are produced. In Israel and elsewhere, weeds bridge the gap as potential perennial host and source of the virus between tomato growing seasons. Figure 2. Tomato yellow leaf curl symptoms on tomato plant. Leaves show yellowing on the edges accompanied by upward curling. Disease control: ,Control of TYLCV is currently based on insecticide treatments and/or physical barriers against the insect vector (Bemisia tabaci), and on tomato breeding programs based on introgression of resistance or tolerance from wild species to cultivated tomato. Useful website: , [source]