Ammonium transporter C of Dictyostelium discoideum is required for correct prestalk gene expression and for regulating the choice between slug migration and culmination

• Published in: Developmental biology 2005-11, Vol.287 (1), p.146-156
• Main Authors: Kirsten, Janet H., Xiong, Yanhua, Dunbar, Andrew J., Rai, Meena, Singleton, Charles K.
• Format: Article
• Language: English
• Subjects: Adenylyl cyclase; Ammonia; Ammonium transporter; Animals; Cation Transport Proteins - genetics; Cation Transport Proteins - physiology; Cell Movement - physiology; Cell Nucleus - metabolism; CudA; DhkC; Dictyostelium; Dictyostelium - genetics; Dictyostelium - physiology; Gene Expression Regulation - physiology; Histidine kinase; Nuclear Proteins - genetics; Nuclear Proteins - metabolism; Phenotype; Phosphorelay; Protein Kinases - biosynthesis; Protein Kinases - genetics; Protozoan Proteins - genetics; Protozoan Proteins - metabolism; Quaternary Ammonium Compounds - metabolism; STAT Transcription Factors - metabolism; STATa; Up-Regulation
• ISSN: 0012-1606; 1095-564X
• DOI: 10.1016/j.ydbio.2005.08.043

Ammonium transporter C (AmtC) is one of three transporters in Dictyostelium that have been proposed to regulate entry and exit of ammonia in a cell type dependent manner and to mediate ammonia signaling. Previous work demonstrated that disruption of the amtC gene results in a slugger phenotype in which the cells remain as migrating slugs when they should form fruiting bodies. More detailed studies on the null strain revealed that differentiation of prestalk cell types was delayed and maintenance of prestalk cell gene expression was defective. There was little or no expression of ecmB, a marker for the initiation of culmination. Normal expression of CudA, a nuclear protein required for culmination, was absent in the anterior prestalk zone. The absence of CudA within the tip region was attributable to the lack of nuclear localization of the transcription factor STATa, despite expression of adenylyl cyclase A mRNA in the slug tips. Disruption of the histidine kinase gene dhkC in the amtC null strain restored STATa and CudA expression and the ability to culminate. The results suggest that the lack of nuclear translocation of STATa results from low cAMP due to a misregulated and overactive DhkC phosphorelay in the amtC null strain.