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Original Articles

Regulation of nitrate reductase in Chlamydomonas reinhardtii by the redox state of the plastoquinone pool

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Pages 345-352 | Received 24 Feb 2005, Accepted 24 Aug 2005, Published online: 20 Feb 2007

Figures & data

Fig. 1. Effect of DCMU and DBMIB on NR activity of Chlamydomonas reinhardtii cells cultured at 100 µmol quanta m−2 s−1. Cells were incubated in the presence of 5 µM DCMU and 1 µM DBMIB for either 6 or 12 h, and enzyme activity in treated cells is shown relative to activity prior to addition of inhibitors (Time 0). Error bars indicate standard deviations (n ≥ 4).

Fig. 1. Effect of DCMU and DBMIB on NR activity of Chlamydomonas reinhardtii cells cultured at 100 µmol quanta m−2 s−1. Cells were incubated in the presence of 5 µM DCMU and 1 µM DBMIB for either 6 or 12 h, and enzyme activity in treated cells is shown relative to activity prior to addition of inhibitors (Time 0). Error bars indicate standard deviations (n ≥ 4).

Fig. 2. Effect of DCMU (5 µM), DBMIB (1 µM) and CCCP (100 µM) on NIA1 expression in Chlamydomonas reinhardtii CC-1692 grown on TP-. Data expressed relative to the control and are means of three different northern gels that were normalized with respect to total RNA. Error bars indicate standard deviations (n = 3; but too small to be visible after 3 h in CCCP).

Fig. 2. Effect of DCMU (5 µM), DBMIB (1 µM) and CCCP (100 µM) on NIA1 expression in Chlamydomonas reinhardtii CC-1692 grown on TP-. Data expressed relative to the control and are means of three different northern gels that were normalized with respect to total RNA. Error bars indicate standard deviations (n = 3; but too small to be visible after 3 h in CCCP).

Fig. 3. A – FRR fluorescence trace of the NIA1 + D1 segregant strain in comparison with the wild-type CC-1692 and the NIA1 D1 mutant (CC-3388). B – upper gel: PCR amplification of NIA1 fragments from NIA1 + wild-type (CC-1692), 2 different isolates of the NIA1 + D1 segregant (CC-1692 + CC-3388), and NIA1 D1 mutant (CC-3388); lower gel: Southern blot carried out on the NIA1 PCR fragments.

Fig. 3. A – FRR fluorescence trace of the NIA1 + D1− segregant strain in comparison with the wild-type CC-1692 and the NIA1 − D1− mutant (CC-3388). B – upper gel: PCR amplification of NIA1 fragments from NIA1 + wild-type (CC-1692), 2 different isolates of the NIA1 + D1− segregant (CC-1692 + CC-3388), and NIA1 − D1− mutant (CC-3388); lower gel: Southern blot carried out on the NIA1 PCR fragments.

Fig. 4. Northern blot showing NIA1 expression in Chlamydomonas reinhardtii CC-1692/CC-3388 A251I (NIA1 + D1) cross incubated in TP in the presence of as the sole N source, and in the presence or absence of 1 µM DBMIB. For both controls and treated cells, samples were collected 3 and 6 h following addition of inhibitor. Upper panel: signal of the NIA1 probe; Lower panel: ethidium bromide dyed northern gel. Equal amounts of total RNA (7.5 µg) were loaded on the northern gel.

Fig. 4. Northern blot showing NIA1 expression in Chlamydomonas reinhardtii CC-1692/CC-3388 A251I (NIA1 + D1−) cross incubated in TP in the presence of as the sole N source, and in the presence or absence of 1 µM DBMIB. For both controls and treated cells, samples were collected 3 and 6 h following addition of inhibitor. Upper panel: signal of the NIA1 probe; Lower panel: ethidium bromide dyed northern gel. Equal amounts of total RNA (7.5 µg) were loaded on the northern gel.

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