Question

1. Most cyanobacteria are photoautotrophs. Some other bacteria are called photoheterotrophs. What do you think this means in terms of metabolic capability and production? Explain. Would you think photoheterotrophs represent an ancestral group of photosynthetic organisms or a more recent group that evolved after the photoautotrophs?

2. Some plants with genetic defects are unable to photorespire. These plants end up being damaged under intense light. Researches identify this as evidence that photorespiration is a protective mechanism in plants. Why might a disabling of the photorespiratory pathway lead to cell damage and how might the process of photorespiration mitigate this damage?

Answer 1

1.CYANOBACTERIA AS PHOTOAUTOTROPHS:

The majority of cyanobacteria are aerobic photoautotrophs. Photoautotrophs are oraganisms that can make their own energy using light and carbon dioxide via the process of photosynthesis. Their life process require only water, carbon dioxide, inorganic substances and light. Photosynthesis is their principal mode of energy metabolism. The use of photosynthetic cyanobacteria to directly convert carbon dioxide to biofuels is an emerging area of interest. They are sources of producing high-valu chemicals, for example pigments, vitamins and enzymes.

CYANOBACTERIA AS PHOTOHETEROTROPHS:

It depends on organic matter already produced by other organisms for its nourishment. Photoheterotrophs obtain their energy from sunlight and carbon from organic material and carbon dioxide. Photo heterotrophs produce ATP through phosphorylation but use environmentally obtained organic compounds to build structures and other bio-molecules. Photoautotrophic organisms are sometimes referred as holophtic.

2. PHOTORESPIRATION:

Plants absorb light for photosynthesis, but this event also damages the photosynthetic machinery, primarily PSII, and it causes photoinactivation of PSII that is referred to as photoinhibition . The photorespiratory pathway has been shown as one of the mechanisms responsible for protecting PSII from photoinhibition .A number of photorespiratory pathway mutants have been isolated by their inability to grow at air versus high CO2 conditions and it has been clearly demonstrated that the photorespiratory pathway is indispensable for growth and survival of C3 plants under current atmospheric conditions.

The photorespiratory pathway consists of dual photorespiratory carbon and nitrogen cycles. It is initiated by the oxygenation of ribulose-1,5-bisphosphate (RuBP) catalyzed by RuBP carboxylase/oxygenase . In this reaction, glycolate-2-P is produced and subsequently metabolized in the photorespiratory carbon cycle to form the Calvin cycle intermediate, glycerate-3-P . During this metabolic process, ammonia is produced by mitochondrial Gly decarboxylase. Ammonia is subsequently refixed into Glu by plastidic isozymes of Gln synthetase and ferredoxin-dependent Glu synthase (Fd-GOGAT) in the photorespiratory nitrogen cycle. Impairment of photorespiratory carbon and nitrogen cycles produces symptoms of light stress, such as photoinhibition and chlorosis, in ambient CO2 but not in conditions that suppress the oxygenase reaction of Rubisco such as high CO2 and/or low oxygen partial pressures, indicating that enzymes of the photorespiratory pathway are indispensable only in conditions where the oxygenase reaction of Rubisco occurs.

The extent of photoinhibition can be seen as a dynamic balance between photodamage to PSII that causes inactivation of PSII and its repair. Therefore, photoinhibition occurs only in conditions where the rate of photodamage exceeds the rate of its repair. To avoid photoinhibition of PSII, photoprotective mechanisms are used by the plant to both suppress the photodamage to PSII and to facilitate the repair of photodamaged PSII. It is believed that consumption of photochemical energy, such as ATP and NADPH, through the photorespiratory pathway helps avoid the photooxidative damage to PSII (acceptor-side photoinhibition) by highly toxic singlet oxygen (1O2) generated via the interaction of oxygen with triplet-excited P680. Thus, the photorespiratory pathway can be seen as a mechanism to minimize the damaging effects of excess light on PSII.

To further understand the role of photorespiration in ameliorating photoinhibition, we have examined the effect of the impairment of the photorespiratory pathway on the photoinhibition process. This was achieved using four Arabidopsis (Arabidopsis thaliana) mutants of the photorespiratory pathway that impair Fd-GOGAT, Ser hydroxymethyltransferase (SHMT), Glu/malate transporter (DiT2), and glycerate kinase (GLYK). Contrary to previous beliefs, impairment of the photorespiratory pathway accelerated photoinhibition by suppression of the repair of photodamaged PSII and not by acceleration of the photodamage to PSII. We found that suppression of the repair was attributable to inhibition of the de novo synthesis of the D1 protein at the translation step. Our results strongly suggest that interruption of the Calvin cycle upon impairment of the photorespiratory pathway causes inhibition of the de novo synthesis of the D1 protein. We conclude that the photorespiratory pathway minimizes photoinhibition by facilitating the repair process (avoiding suppression of the repair of photodamaged PSII) but not by suppressing the photodamage process.