Degradation of the cyanobacterial light-harvesting antenna, the
phycobilisome, is a general acclimation response that is observed under various stress conditions. In this study we identified a novel mutant of Synechococcus elongatus PCC 7942 that exhibits impaired
phycobilisome degradation specifically during
nitrogen starvation, unlike previously described mutants, which exhibit aberrant degradation under
nitrogen,
sulfur, and
phosphorus starvation conditions. The phenotype of the new mutant, AldOmega, results from inactivation of ald (encoding
alanine dehydrogenase). AldOmega is deficient in transcription induction of a number of genes during
nitrogen starvation. These genes include the "general nutrient stress-related" genes, nblA and nblC, the products of which are essential for
phycobilisome degradation. Furthermore, transcripts of several specific
nitrogen-responsive genes accumulate at lower levels in AldOmega than in the wild-type strain. In contrast, ald inactivation did not decrease the accumulation of transcripts during
sulfur starvation. Transcription of ald is induced upon
nitrogen starvation, which is consistent with the ability of wild-type cells to maintain a low cellular content of
alanine under these conditions. Unlike wild-type cells, AldOmega accumulates
alanine upon
nitrogen starvation. Our analyses suggest that
alanine dehydrogenase activity is necessary for an adequate cellular response to
nitrogen starvation. Decomposition of
alanine may be required to provide a sufficient amount of
ammonia. Furthermore, the accumulated
alanine, or a related metabolite, may interfere with the cues that modulate acclimation during
nitrogen starvation. Taken together, our results provide novel information regarding cellular responses to
nitrogen starvation and suggest that mechanisms related to
nitrogen-specific responses are involved in modulation of a general acclimation process.