| Literature DB >> 26651943 |
Alessandro D Uboldi1, James M McCoy1, Martin Blume2, Motti Gerlic1, David J P Ferguson3, Laura F Dagley1, Cherie T Beahan4, David I Stapleton5, Paul R Gooley2, Antony Bacic4, Seth L Masters1, Andrew I Webb1, Malcolm J McConville2, Christopher J Tonkin6.
Abstract
Transmissible stages of Toxoplasma gondii store energy in the form of the carbohydrate amylopectin. Here, we show that the Ca(2+)-dependent protein kinase CDPK2 is a critical regulator of amylopectin metabolism. Increased synthesis and loss of degradation of amylopectin in CDPK2 deficient parasites results in the hyperaccumulation of this sugar polymer. A carbohydrate-binding module 20 (CBM20) targets CDPK2 to amylopectin stores, while the EF-hands regulate CDPK2 kinase activity in response to Ca(2+) to modulate amylopectin levels. We identify enzymes involved in amylopectin turnover whose phosphorylation is dependent on CDPK2 activity. Strikingly, accumulation of massive amylopectin granules in CDPK2-deficient bradyzoite stages leads to gross morphological defects and complete ablation of cyst formation in a mouse model. Together these data show that Ca(2+) signaling regulates carbohydrate metabolism in Toxoplasma and that the post-translational control of this pathway is required for normal cyst development.Entities:
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Year: 2015 PMID： 26651943 DOI： 10.1016/j.chom.2015.11.004
Source DB: PubMed Journal: Cell Host Microbe ISSN： 1931-3128 Impact factor: 21.023