Disease relevance of glnA

• This site showed extensive sequence similarity with the promoter region of glnA from Synechococcus sp. strain PCC 7942 [1].
• A transcription start point of the Anabaena glnA gene (corresponding to RNAl), that has been shown to be used preferentially after nitrogen step-down, was not used in the ntcA insertional mutant [2].
• A Synechocystis sp. glnA mutant could not be obtained, however, from the wild-type Synechocystis sp. The Anabaena glutamine synthetase enzyme was subject to ammonium-promoted inactivation when expressed in the Synechocystis strain but not in the Anabaena strain itself [3].
• In the filamentous, N(2)-fixing cyanobacterium 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 [4].
• Molecular characteristics of glnA linked mutations in the nitrogen-fixing cyanobacterium Nostoc muscorum [5].

High impact information on glnA

• In the ntcA mutant, in response to removal of ammonium, accumulation of mRNA of the genes encoding nitrogenase (nifHDK), nitrite reductase (nir, the first gene of the nitrate assimilation operon), and glutamine synthetase (glnA) was not observed [2].
• Expression of the glnA gene encoding glutamine synthetase, a key enzyme in nitrogen metabolism, is subject to a variety of regulatory mechanisms in different organisms [4].
• The NtcA-binding site in the P(1) promoter and binding of NtcA to this site appear to be key factors in determining glnA gene expression in vegetative cells and heterocysts [4].
• The binding site is between the major glnA transcription start site used in vegetative cells (RNAII) and the major transcription start site used under nitrogen-deficient conditions (RNAI) [6].
• A strain derived from Synechocystis sp. strain PCC 6803 which contained integrated into the chromosome, in addition to its own glnA gene, the Anabaena glnA gene was constructed [3].

Chemical compound and disease context of glnA

• The glutamine synthetase (GS)-impaired mutants of Nostoc muscorum, isolated as ethylenediamine (EDA) resistant phenotype, were characterized for glnA linked processes to investigate the molecular mechanism of GS impairment [5].

Biological context of glnA

• Morphological analyses revealed differences between the free-living isolates and their symbiotic counterparts, as did restriction fragment length polymorphism (RFLP) analyses with both single-copy glnA and rbcS gene probes and a multicopy psbA gene probe [7].
• Results suggested that point mutation(s) inflicted in glnA gene of N. muscorum are responsible for differential production of catalytically modified GS in EDA-resistant phenotypes [5].

Other interactions of glnA

• Northern analysis of RNA samples isolated from ammonium-grown cultures of the ntcA mutant showed reduced amounts of glnA message and the absence of a 1.7-kb transcript [8].
• We also show that the levels of these psbB gene transcripts as well as those of the glnA, rbcLS, and psbA genes, in RNA prepared from whole filaments, remain constant during heterocyst differentiation [9].
• Using the Southern blot technique and cloned Anabaena PCC 7120 nifK and glnA genes as probes, restriction fragment length polymorphisms of these cyanobacterial symbionts were compared [10].

Analytical, diagnostic and therapeutic context of glnA

• Northern blot analysis indicated differential levels of GS specific mRNA and abundance of glnA transcripts of 1.7 and 1.9 kb in the mutant strains [5].

References