Mio Sato-Cruz

  • Apr 17, 2018

Date & Location: April 17, 2018, at 12p; Room 168 Plant Biology Building

Subject: A novel modulator of the chloroplast ATP synthase: implications for regulation of photosynthesis

Abstract: The light reactions of photosynthesis are coordinated by regulation of the chloroplast ATP synthase, which governs the buildup of the thylakoid proton motive force. In recent work we found evidence that the ATP synthase is regulated both at the enzyme level (by allosteric factors) and by modulating the expression level of the complex.

Using a combination of forward and reverse genetics and high throughput phenotyping, we identified a new factor MAAC6 (modified ATP synthase activity and content) that when inactivated leads to strong decreases in ATP synthase content and activity. During photosynthesis, maac6 shows high pmf and hyperactivation of the photoprotective qE response. Maac6 encodes a chloroplast stromal protein of unknown function that is conserved in higher plants. Expression and turnover analyses ruled out effects on regulation at the levels of transcription or degradation. One possible hypothesis is that Maac6 is an ATP synthase assembly factor, however, we see no evidence for accumulation of partially assembled complexes (as seen with mutants defective in other ATP synthase assembly factors).

More interesting, over-expression (OE) of MAAC6 leads to large accumulation of the complete ATP synthase complex, suggesting a role in regulating ATP synthase content. However, the in vivo activity of the complex was not increased in OE lines, consistent with previous work suggesting that a large pool of the ATP synthase is inactive, and possibly involved in regulation. We also found evidence for the involvement of MAAC6 in redox regulation. One unique feature of MAAC6 is that it contains 3 conserved cysteine residues which may play a role in redox regulation. Further, maac6 mutant lines show increased protein levels of the soluble form of Ferredoxin-NADP(+) reductase (FNR), which is known to play a role in redox regulation of cyclic electron flow.  Hence, it appears that FNR may be compensating for the lack of MAAC6 in maac6 mutant lines. Consequently, we propose that MAAC6 plays an important role in regulation of ATP synthase content by acting as a stromal redox sensor.

Mio Sato-Cruz is a student/post-doc in the lab of David Kramer.