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71.
The Tsc/Rheb signaling pathway plays critical roles in the control of growth and cell cycle. Studies in fission yeast have
also implicated its importance in the regulation of amino acid uptake. Disruption of tsc2
+, one of the tsc
+ genes, has been shown to result in decreased arginine uptake and resistance to canavanine. A similar effect is also seen
with other basic amino acids. We have identified a permease responsible for the uptake of basic amino acids by genetic complementation
and disruption. SPAC869.11 (termed Cat1 for cationic amino acid transporter) contains 12 predicted transmembrane domains and
its overexpression in wild type fission yeast leads to the increased uptake of basic amino acids and sensitivity to canavanine.
Disruption of cat1
+ in the Δtsc2 background interfered with the suppression of the canavanine-resistant phenotype of Δtsc2 mutants by a dominant negative Rheb. In Δtsc2 mutant strains, the amount of Cat1 was not altered, but instead was mislocalized. This mislocalization was suppressed by
the expression of dominant negative Rheb. In addition, we found that the loss of the E3 ubiquitin ligase, Pub1, also restores
proper localization. These results provide a crucial link between Tsc/Rheb signaling and the regulation of the basic amino
acid permease in fission yeast. 相似文献
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Urano J Comiso MJ Guo L Aspuria PJ Deniskin R Tabancay AP Kato-Stankiewicz J Tamanoi F 《Molecular microbiology》2005,58(4):1074-1086
Rheb GTPase is a key player in the control of growth, cell cycle and nutrient uptake that is conserved from yeast to humans. To further our understanding of the Rheb pathway, we sought to identify hyperactivating mutations in the Schizosaccharomyces pombe Rheb, Rhb1. Hyperactive forms of Rhb1 were found to result from single amino acid changes at valine-17, serine-21, lysine-120 or asparagine-153. Expression of these mutants confers resistance to canavanine and thialysine, phenotypes which are similar to phenotypes exhibited by cells lacking the Tsc1/Tsc2 complex that negatively regulates Rhb1. The thialysine-resistant phenotype of the hyperactive Rhb1 mutants is suppressed by a second mutation in the effector domain. Purified mutant proteins exhibit dramatically decreased binding of GDP, while their GTP binding is not drastically affected. In addition, some of the mutant proteins show significantly decreased GTPase activities. Thus the hyperactivating mutations are expected to result in an increase in the GTP-bound/GDP-bound ratio of Rhb1. By using the hyperactive mutant, Rhb1(K120R), we have been able to demonstrate that Rhb1 interacts with Tor2, one of the two S. pombe TOR (Target of Rapamycin) proteins. These fission yeast results provide the first evidence for a GTP-dependent association of Rheb with Tor. 相似文献
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Sarfraz A Tunio Neil J Oldfield Dlawer AA Ala'Aldeen Karl G Wooldridge David PJ Turner 《BMC microbiology》2010,10(1):280
Background
Glyceraldehyde 3-phosphate dehydrogenases (GAPDHs) are cytoplasmic glycolytic enzymes, which although lacking identifiable secretion signals, have also been found localized to the surface of several bacteria (and some eukaryotic organisms); where in some cases they have been shown to contribute to the colonization and invasion of host tissues. Neisseria meningitidis is an obligate human nasopharyngeal commensal which can cause life-threatening infections including septicaemia and meningitis. N. meningitidis has two genes, gapA-1 and gapA-2, encoding GAPDH enzymes. GapA-1 has previously been shown to be up-regulated on bacterial contact with host epithelial cells and is accessible to antibodies on the surface of capsule-permeabilized meningococcal cells. The aims of this study were: 1) to determine whether GapA-1 was expressed across different strains of N. meningitidis; 2) to determine whether GapA-1 surface accessibility to antibodies was dependant on the presence of capsule; 3) to determine whether GapA-1 can influence the interaction of meningococci and host cells, particularly in the key stages of adhesion and invasion. 相似文献77.
The complete mitochondrial DNA sequence of the shark Mustelus manazo: evaluating rooting contradictions to living bony vertebrates 总被引:5,自引:0,他引:5
A remarkable example of a misleading mitochondrial protein tree is
presented, involving ray-finned fishes, coelacanths, lungfishes, and
tetrapods, with sea lampreys as an outgroup. In previous molecular
phylogenetic studies on the origin of tetrapods, ray-finned fishes have
been assumed as an outgroup to the tetrapod/lungfish/coelacanth clade, an
assumption supported by morphological evidence. Standard methods of
molecular phylogenetics applied to the protein-encoding genes of
mitochondria, however, give a bizarre tree in which lamprey groups with
lungfish and, therefore, ray-finned fishes are not the outgroup to a
tetrapod/lungfish/coelacanth clade. All of the dozens of published
phylogenetic methods, including every possible modification to maximum
likelihood known to us (such as inclusion of site heterogeneity and
exclusion of potentially misleading hydrophobic amino acids), fail to place
the ray-finned fishes in a biologically acceptable position. A likely cause
of this failure may be the use of an inappropriate outgroup. Accordingly,
we have determined the complete mitochondrial DNA sequence from the shark,
Mustelus manazo, which we have used as an alternative and more proximal
outgroup than the lamprey. Using sharks as the outgroup, lungfish appear to
be the closest living relative of tetrapods, although the possibility of a
lungfish/coelacanth clade being the sister group of tetrapods cannot be
excluded.
相似文献
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79.
Decomposable graphical Gaussian model determination 总被引:8,自引:0,他引:8