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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 
 

Expression of protein tyrosine phosphatase-like molecule ICA512/ IA-2 induces growth arrest in yeast cells and transfected mammalian cell lines.

The ICA512/ IA-2 molecule, a protein with similarity to receptor-type protein tyrosine phosphatases, was discovered during studies to identify autoantigens in Type 1 diabetes. The biological function of ICA512/ IA-2 is unknown. We describe striking effects of ICA512/ IA-2 on viability and growth of both yeast cells and cultured mammalian cells. In transformed yeast Saccharomyces cerevisiae cells, expression of ICA512/ IA-2 induced growth retardation as judged by measurements of optical density and counts of colony-forming units. In contrast, expression of the intracellular domain (amino acids 600-979) of ICA512/ IA-2 in yeast or mammalian cells had no such effects. In investigations on apoptosis, expression of ICA512/ IA-2 in yeast cells caused loss of plasma membrane asymmetry, but not release of cytochrome c from mitochondria which did occur in a control system after expression of the pro-apoptotic molecule Bax. Possible interactions between ICA512/ IA-2 and components of the cytoskeleton were not supported by studies on staining of fixed yeast cells with phalloidin-Texas Red. With transfected mammalian cell lines COS-7 and NIH3T3, expression of ICA512/ IA-2 likewise induced growth arrest, with some of the morphological features of apoptosis. Thus obligatory expression of ICA512/ IA-2 in eukaryotic cells causes disruption of cellular activities, with growth arrest in yeast and nuclear pycnosis/fragmentation in mammalian cells. A possible explanation is that growth inhibition reflects a part of the presently unknown function of ICA512/ IA-2.[1]

References

  1. Expression of protein tyrosine phosphatase-like molecule ICA512/IA-2 induces growth arrest in yeast cells and transfected mammalian cell lines. Papakonstantinou, T., Myers, M.A., Jois, J., Roucou, X., Prescott, M., Rowley, M.J., Mackay, I.R. J. Autoimmun. (2001)
 
 
 
 
 
 
 
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