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  • National Academy of Sciences  (2)
  • The Federation of American Societies for Experimental Biology (FASEB)  (1)
  • 1
    Publikationsdatum: 2011-11-09
    Beschreibung: We identified an Arabidopsis thaliana mutant, clumped chloroplasts 1 (clmp1), in which disruption of a gene of unknown function causes chloroplasts to cluster instead of being distributed throughout the cytoplasm. The phenotype affects chloroplasts and nongreen plastids in multiple organs and cell types, but is detectable only at certain developmental stages. In young leaf petioles of clmp1, where clustering is prevalent, cells lacking chloroplasts are detected, suggesting impaired chloroplast partitioning during mitosis. Although organelle distribution and partitioning are actin-dependent in plants, the actin cytoskeleton in clmp1 is indistinguishable from that in WT, and peroxisomes and mitochondria are distributed normally. A CLMP1-YFP fusion protein that complements clmp1 localizes to discrete foci in the cytoplasm, most of which colocalize with the cell periphery or with chloroplasts. Ultrastructural analysis revealed that chloroplasts within clmp1 clusters are held together by membranous connections, including thin isthmi characteristic of late-stage chloroplast division. This finding suggests that constriction of dividing chloroplasts proceeds normally in clmp1, but separation is impaired. Consistently, chloroplast size and number, as well as positioning of the plastid division proteins FtsZ and ARC5/DRP5B, are unaffected in clmp1, indicating that loss of CLMP1-mediated chloroplast separation does not prevent otherwise normal division. CLMP1-like sequences are unique to green algae and land plants, and the CLMP1 sequence suggests that it functions through protein–protein interactions. Our studies identify a unique class of proteins required for plastid separation after the constriction stage of plastid division and indicate that CLMP1 activity is also required for plastid distribution and partitioning during cell division.
    Print ISSN: 0027-8424
    Digitale ISSN: 1091-6490
    Thema: Biologie , Medizin , Allgemeine Naturwissenschaft
    Standort Signatur Einschränkungen Verfügbarkeit
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  • 2
    Publikationsdatum: 2014-10-08
    Beschreibung: The highly structured (64% GC) covalently closed circular (CCC) RNA (220 nt) of the virusoid associated with rice yellow mottle virus codes for a 16-kDa highly basic protein using novel modalities for coding, translation, and gene expression. This CCC RNA is the smallest among all known viroids and virusoids and...
    Print ISSN: 0027-8424
    Digitale ISSN: 1091-6490
    Thema: Biologie , Medizin , Allgemeine Naturwissenschaft
    Standort Signatur Einschränkungen Verfügbarkeit
    BibTip Andere fanden auch interessant ...
  • 3
    Publikationsdatum: 2015-07-01
    Beschreibung: Cigarette smoke (CS)-induced cellular senescence is involved in the pathogenesis of chronic obstructive pulmonary disease (COPD). The molecular mechanism by which CS induces cellular senescence is unknown. Here, we show that CS stress (exposure of primary lung cells to CS extract 0.2–0.75% with a half-maximal inhibitory concentration of ~0.5%) led to impaired mitophagy and perinuclear accumulation of damaged mitochondria associated with cellular senescence in both human lung fibroblasts and small airway epithelial cells (SAECs). Impaired mitophagy was attributed to reduced Parkin translocation to damaged mitochondria, which was due to CS-induced cytoplasmic p53 accumulation and its interaction with Parkin. Impaired Parkin translocation to damaged mitochondria was also observed in mouse lungs with emphysema (6 months CS exposure, 100 mg TPM/m 3 ) as well as in lungs of chronic smokers and patients with COPD. Primary SAECs from patients with COPD also exhibited impaired mitophagy and increased cellular senescence via suborganellar signaling. Mitochondria-targeted antioxidant (Mito-Tempo) restored impaired mitophagy, decreased mitochondrial mass accumulation, and delayed cellular senescence in Parkin-overexpressing cells. In conclusion, defective mitophagy leads to CS stress-induced lung cellular senescence, and restoring mitophagy delays cellular senescence, which provides a promising therapeutic intervention in chronic airway diseases.—Ahmad, T., Sundar, I. K., Lerner, C. A., Gerloff, J., Tormos, A. M., Yao, H., Rahman, I. Impaired mitophagy leads to cigarette smoke stress-induced cellular senescence: implications for chronic obstructive pulmonary disease.
    Print ISSN: 0892-6638
    Digitale ISSN: 1530-6860
    Thema: Biologie
    Standort Signatur Einschränkungen Verfügbarkeit
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