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Por favor, use este identificador para citar o enlazar a este item: http://hdl.handle.net/10261/111855
Título

The NtcA-dependent P1 promoter is utilized for glnA expression in N2-fixing heterocysts of Anabaena sp. strain PCC 7120

AutorValladares, Ana ; Muro-Pastor, Alicia M.; Herrero, Antonia ; Flores, Enrique
Fecha de publicación2004
EditorAmerican Society for Microbiology
CitaciónJournal of Bacteriology 186: 7337- 7343 (2004)
ResumenExpression of the glnA gene encoding glutamine synthetase, a key enzyme in nitrogen metabolism, is subject to a variety of regulatory mechanisms in different organisms. In the filamentous, N2-fixing cyanobacteritim Anabaena sp. strain PCC 7120, glnA is expressed from multiple promoters that generate several transcripts whose abundance is influenced by NtcA, the transcription factor exerting global nitrogen control in cyanobacteria. Whereas RNAI originates from a canonical NtcA-dependent promoter (P 1) and RNAII originates from a σ70-type promoter (P2), RNAIV is influenced by NtcA but the corresponding promoter (P3) does not have the structure of NtcA-activated promoters. Using RNA isolated from Anabaena filaments grown under different nitrogen regimens, we observed, in addition to these transcripts, RNAV, which has previously been detected only in in vitro transcription assays and should originate from P4. However, in heterocysts, which are differentiated cells specialized in N2 fixation, RNAI was the almost exclusive glnA transcript. Analysis of PglnA::lacZ fusions containing different fragments of the glnA upstream region confirmed that fragments carrying P1, P2, or P3 and P4 have the ability to promote transcription. Mutation of the NtcA-binding site in P1 eliminated P 1-directed transcription and allowed increased use of P2. The NtcA-binding site in the P1 promoter and binding of NtcA to this site appear to be key factors in determining glnA gene expression in vegetative cells and heterocysts.
URIhttp://hdl.handle.net/10261/111855
DOI10.1128/JB.186.21.7337-7343.2004
Identificadoresdoi: 10.1128/JB.186.21.7337-7343.2004
issn: 0021-9193
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