The Anabaena sp. strain PCC 7120 ntcA gene showed multiple transcripts with different 5 ends. The relative abundance of transcripts varied in response to nitrogen availability. The ntcA product, NtcA, showed binding to the promoter region of its own gene. The binding site mapped to a region between the transcription start site used under nitrogen-replete conditions and the start sites used under nitrogen-limiting conditions, suggesting that NtcA regulates its own expression.

The persistence of circulating auto-antibodies is indicative of a breach in B cell tolerance. Mice that constitutively over-expressed the transcription factor Bright throughout B cell development produced antibodies to nuclear antigens (ANAs) similar to those produced in autoimmune diseases such as lupus. Whereas, normal mice reduce Bright expression in mature B cells and do not produce ANAs. ANAs did not result from global hyperglobulinemia and were IgG demonstrating that they originated from B cells that had transited the germinal center. ANA production was dependent upon Bruton's tyrosine kinase. To determine where tolerance breaches occurred in this autoimmune model, we analyzed transgenic B cells for abnormalities at multiple tolerance checkpoints. We found that early transitional B cells responded to BCR stimulation with exaggerated cell death, suggesting the clonal deletion checkpoint was in tact. Transgenic mice also developed normal numbers of naturally occurring anergic B cells. Interestingly, mature B cell numbers were down by half and those cells were hyper-responsive to proliferative signals. The marginal zone compartment is enriched for self reactive B cell. A bias towards marginal zone versus follicular B cell development was evident both in cell numbers and through crosses with Bcl2 transgenics. Together, these data suggest that appropriate regulation of Bright levels is critical for maintaining normal B cell tolerance.