Osmotic stabilizer-coupled suppression of NDR defects is dependent on the calcium-calcineurin signaling cascade in Aspergillus nidulans.

Establishment and maintenance of cell polarity are coordinated by signaling pathways such as NDR (nuclear Dbf2-related) protein-kinase signaling and calcium signaling pathway. The NDR family of kinase is structurally related to the human myotonic dystrophy kinase, which, when impaired, confers a disease that involves changes in cytoarchitecture and ion homeostasis. CotA kinase, a member of the NDR protein kinase family, forms a complex with MobB to regulate cell polarized growth in Aspergillus nidulans. Our previous study demonstrated that mobB/cotA defects could be suppressed by the osmotic stress in the presence of external calcium. In this study, via the genetic and molecular approach, we further demonstrated that Ca(2+)-permeable stretch-activated nonselective cation channel-MidA, calcium/calmodulin-dependent protein phosphatase catalatic subunit-CnaA and external calcium, but not voltage-gated calcium channel homolog-CchA, were required for the osmotic stabilizer-coupled suppression. The up-regulation of calcium/calcineurin signaling pathway induced by osmotic stress might be the reason for bypassing the requirements of NDR kinase complex, which is otherwise necessary for polar morphogenesis. Our results suggest that calcium-calcineurin signaling pathway coordinates with MobB/CotA kinase complex in regulating polarity growth via maintaining cellular calcium homeostasis. However, CchA may act differently as other components in calcium signaling pathway in Aspergillus nidulans. These findings provide an excellent opportunity to identify the potential pathway linking NDR protein-kinase network to calcium signaling pathway.