Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0038187 (starvation)
 24,951 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A cluster of pathogenicity genes ( PEP1, PEP2, PDA1, PEP5), termed the pea pathogenicity ( PEP) cluster and located on a 1.6-Mb conditionally dispensable (CD) chromosome, was identified in the fungal pathogen Nectria haematococca. Studies determined that the expression of PDA1 is induced in both infected pea tissues and in vitro by the phytoalexin pisatin. The present study reports the use of real-time quantitative RT-PCR to monitor the expression of each PEP gene and PDA1. In mycelia actively growing in culture, the mRNA levels of PEP1, PEP5 and PDA1 were very low and the PEP2 transcript was undetectable. In planta, PDA1 and PEP2 were strongly induced, while PEP1 and PEP5 were moderately induced. Starvation slightly enhanced the expression of PEP1, PDA1 and PEP5, while the expression of PEP2 remained undetectable. Exposure to pisatin in culture stimulated the expression of PDA1 and each PEP gene to a similar level as occurred in planta. In addition, all four pathogenicity genes displayed similar temporal patterns of expression in planta and in vitro, consistent with a coordinated regulation of these genes by pisatin during pea pathogenesis. In the flanking regions of the PEP cluster, six open reading frames (ORFs) were identified and all were expressed during infection of pea. Comparison of the codon preferences of these ORFs and seven additional genes from CD chromosomes with the codon preferences of 21 genes from other chromosomes revealed there is a codon bias that correlates with the source of the genes. This difference in codon bias is consistent with the hypothesis that genes on the CD chromosome have a different origin from genes of normal chromosomes, suggesting that horizontal gene transfer may have played a role in the evolution of pathogenesis in N. haematococca.
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PMID:Expression profiles of pea pathogenicity ( PEP) genes in vivo and in vitro, characterization of the flanking regions of the PEP cluster and evidence that the PEP cluster region resulted from horizontal gene transfer in the fungal pathogen Nectria haematococca. 1292 99

Homotypic fusion and vacuole protein sorting (HOPS) is a tethering complex required for trafficking to the vacuole/lysosome in yeast. Specific interaction of HOPS with certain SNARE (soluble NSF attachment protein receptor) proteins ensures the fusion of appropriate vesicles. HOPS function is less well characterized in metazoans. We show that all six HOPS subunits (Vps11 [vacuolar protein sorting 11]/CG32350, Vps18/Dor, Vps16A, Vps33A/Car, Vps39/CG7146, and Vps41/Lt) are required for fusion of autophagosomes with lysosomes in Drosophila. Loss of these genes results in large-scale accumulation of autophagosomes and blocks autophagic degradation under basal, starvation-induced, and developmental conditions. We find that HOPS colocalizes and interacts with Syntaxin 17 (Syx17), the recently identified autophagosomal SNARE required for fusion in Drosophila and mammals, suggesting their association is critical during tethering and fusion of autophagosomes with lysosomes. HOPS, but not Syx17, is also required for endocytic down-regulation of Notch and Boss in developing eyes and for proper trafficking to lysosomes and eye pigment granules. We also show that the formation of autophagosomes and their fusion with lysosomes is largely unaffected in null mutants of Vps38/UVRAG (UV radiation resistance associated), a suggested binding partner of HOPS in mammals, while endocytic breakdown and lysosome biogenesis is perturbed. Our results establish the role of HOPS and its likely mechanism of action during autophagy in metazoans.
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PMID:Interaction of the HOPS complex with Syntaxin 17 mediates autophagosome clearance in Drosophila. 2455 66