例如:"lncRNA", "apoptosis", "WRKY"

Golgi self-correction generates bioequivalent glycans to preserve cellular homeostasis.

Elife. 2016 Jun 08;5. doi:10.7554/eLife.14814
Haik Mkhikian 1 , Christie-Lynn Mortales 1 , Raymond W Zhou 2 , Khachik Khachikyan 1 , Gang Wu 3 , Stuart M Haslam 3 , Patil Kavarian 1 , Anne Dell 3 , Michael Demetriou 2
Haik Mkhikian 1 , Christie-Lynn Mortales 1 , Raymond W Zhou 2 , Khachik Khachikyan 1 , Gang Wu 3 , Stuart M Haslam 3 , Patil Kavarian 1 , Anne Dell 3 , Michael Demetriou 2
+ et al

[No authors listed]

Author information
  • 1 Department of Microbiology and Molecular Genetics, University of California, Irvine, United States.
  • 2 Department of Neurology and Institute for Immunology, University of California, Irvine, United States.
  • 3 Department of Life Sciences, Imperial College London, London, United Kingdom.

摘要


Essential biological systems employ self-correcting mechanisms to maintain cellular homeostasis. Mammalian cell function is dynamically regulated by the interaction of cell surface galectins with branched N-glycans. Here we report that N-glycan branching deficiency triggers the Golgi to generate bioequivalent N-glycans that preserve galectin-glycoprotein interactions and cellular homeostasis. Galectins bind N-acetyllactosamine (LacNAc) units within N-glycans initiated from UDP-GlcNAc by the medial-Golgi branching enzymes as well as the trans-Golgi poly-LacNAc extension enzyme β1,3-N-acetylglucosaminyltransferase (B3GNT). Marginally reducing LacNAc content by limiting N-glycans to three branches results in T-cell hyperactivity and autoimmunity; yet further restricting branching does not produce a more hyperactive state. Rather, new poly-LacNAc extension by B3GNT maintains galectin binding and immune homeostasis. Poly-LacNAc extension is triggered by redistribution of unused UDP-GlcNAc from the medial to trans-Golgi via inter-cisternal tubules. These data demonstrate the functional equivalency of structurally dissimilar N-glycans and suggest a self-correcting feature of the Golgi that sustains cellular homeostasis.

KEYWORDS: Golgi, N-glycosylation, T cell, biochemistry, bioequivalence, cell biology, galectin, human, mouse, self-correction