Throughout our extensive unit on photosynthesis/cellular respiration, the aforementioned concepts were hammered into our memories through multiple packets and instructive videos. By the end of the aforementioned section/topic, I was certain that we had hit every single key point of cellular metabolism in relation to plants and other autotrophs – until I unexpectedly bumped into the concept of photorespiration while flipping through the Campbell book. The concept also surfaced in one of our class discussions regarding the basics of CAM and C4 plants (chalk exercises), inciting further fascination. After closer inspection, I deduced that photorespiration describes a metabolic path way in which Rubisco bonded RuBP with O2 (instead of the usual Co2) resulting in a seemingly useless product; the production of the O2-RuBP product requires input of energy (for the precursory reactions) without generating any ATP in return (it’s missing the crucial carbon source conventionally found in the CO2). Slightly confused and even more so curious regarding the counterintuitive process of photorespiration, the aforementioned topic caught my attention in the evolutionary context: why has photorespiration survived evolutionary selection if the process required more ATP than it produced? Shouldn’t evolution have shunted photorespiration out of existence if the process was metabolically draining and even fatal to plants? The remainder of this blog post explores the evolutionary benefits of photorespiration and the fundamental reasons to its survival throughout the spectrum of time.
As briefly aforementioned, the term “photorespiration” describes the rare scenario when either Co2 levels are too low and/or O2 levels are extraordinarily high within the plant. In either of these conditions, the carbon fixation with the Ribulose Phosphate (RuBP) fails to occur; instead, Rubisco mistakenly binds O2 with RuBP. Unfortunately, the complete lack of carbon within O2 deprives the Calvin-Benson Cycle of the necessary carbon that constitutes C6H12O6, preventing the creation of glucose and ultimately depriving the plant of necessary energy storing molecules. Fortunately, photorespiration exists as a rare phenomenon, with certain beneficial uses under specific conditions. Explored extensively within Wingler, Lea, Quick, and Leegood’s Photorespiration: metabolic pathways and their role in stress protection, the process of photorespiration provides three crucial impacts to plant function: glutathione production, drought protection, and excess light protection – all explored below. The first key implication of photorespiration involves the metabolic production of glutathione as a byproduct of the RuBP-O2 product. Catherine Gutherie of Experience Life Magazines describes glutathione “as [a peptide that] protects the cell’s engine, called the mitochondria, from bacteria and viruses as well as toxins. It’s considered “the mother of all antioxidants,” as Hyman calls it, because all other antioxidants, including vitamin C and vitamin E, rely on it to give them a second life. The average antioxidant has a short life span, sacrificing itself whenever it wipes out a free radical. But glutathione carries enough extra zip to not only bring spent antioxidants back from the dead but also to recharge itself, explains Leslie Fuller, ND, an educator at the National College of Natural Medicine and practitioner at the Nature Cures Clinic, both in Portland, Ore” (Gutherie 2011) This “mother of all antioxidants” as dubbed by Gutherie/Hyman is absolutely crucial to all cellular life as it combats and mitigates the effects of oxygen free radicals. Oxygen free radicals are molecules that are missing electrons. In a desperate and frantic attempt to acquire the missing electron(s), these “free radicals” forcefully steal subatomic particles from neighboring molecules, disrupting chemical composition and hence function. Antioxidants can be perceived as the cell’s protector: it acts to neutralize the free radicals, preventing the pesky molecules from “stealing” other electrons. As Gutherie describes, glutathione allows for recharging of other antioxidants (Vit C, Vit E, etc.) that allow for further “combat” against the destructive free radicals. With the aforementioned in mind, researchers Wingler, Lea, Quick and Leegood found in their study of GS2 mutant plants and implications of photorespiration that: “Photorespiratory metabolites can be provided as substrates for other processes (Keys 1999). Glycine produced in the photorespiratory pathway can be used for the synthesis of glutathione [an important antioxidant used by plants to prevent damage from reactive oxygen radicals, free radicals, and peroxides] (Noctor et al. 1997, 1998, 1999) or be exported out of the leaves (Madore & Grodzinski 1984). Some flexibility in photorespiratory nitrogen metabolism is achieved by the use of alternative amino donors. In addition to [photorespiration-generated] glutamate and serine, alanine and asparagine provide amino nitrogen for the synthesis of glycine” (Astrid Wingler, Peter J. Lea, W. Paul Quick, and Richard C. Leegood 2000). Thus during the process of photorespiration, glutathione and other essential amino acids (glutamate, serine, alanine, asparagine) are formed from the byproducts of the RuBP-O2 reaction, allowing for the production of essential antioxidants for the afflicted plants. In turn, these antioxidants provide an elevation in protection against oxidization and the disruptive effects of oxygen free radicals, allowing for plant health and efficient functioning.
In addition to the beneficial impacts of anti-oxidant production, photorespiration provides for two additional lines of defense against external influences of drought and light. In each of the two scenarios, a lack of carbon fixation prevents the continuation of electron flow, causing for the build-up of high energy (unstable) carrier molecules, ultimately leading to plant tissue harm. In the former situation, drought stress prevents the opening of stomata; with water retention already a huge concern in levels of low precipitation, water cannot not be further lost through transpiration. Hence the plant is forced to close their stomata. Unfortunately, the closing of stomata also implies a lack of Co2 flowing into the plant (due to the blockage in gas exchange), preventing the Calvin cycle from occurring. The charged and reactive NADPH and ATP molecules that would originally deposit their energy for the formation of PGA/G3P find themselves with nowhere to go – the Calvin cycle is literally at a standstill due to the lack of Co2. Thus photorespiration (RuBP + O2) performs the role of accepting the energy from ATP and NAPDH, preventing any further tissue damage from excess energy. The London team of researchers confirms the aforementioned theoretical process by finding that “Long term, drought stress has, however, been shown to result in lower fructose-1,6-bisphosphatase activities and a decline in the amounts of sedoheptulose-1,7-bisphosphatase and NADP-dependent glyceraldehyde-3-phosphate dehydrogenase proteins (Wingler et al. 1999b). [However]. the amounts of photo respiratory enzyme proteins (proteins of the GDC complex, GS-2, SGAT) were not affected by drought stress. Therefore, photorespiration could serve as an important means to maintain electron flow; with decreasing rates of CO2 assimilation almost linearly in the wild-type, the mutants with reduced activities of photorespiratory enzymes accelerated [this decrease], resulting in lower rates of CO2 assimilation at moderate drought stress [compared to with photorespiration]” (Astrid Wingler, Peter J. Lea, W. Paul Quick, and Richard C. Leegood 2000). Hence, photorespiration provides for significant drought stress alleviation by providing a “drop off zone” for energy carrier molecules reduced from the light dependent reactions. Under dramatic situations and utilized sparingly, photorespiration proves to be less of a detriment and more as a mode of protection against drought/Co2 depletion. The same logic applies to excess light, where the plant absorbs too many photons of light but lacks sufficient Co2 to fix during the Calvin Cycle. In order to oxidize ATP and NADPH for the prevention of over accumulation and tissue damage, photorespiration provides for a way to “use up” excess energy without producing glucose. What’s even more, the evolutionary selection for plants capable of utilizing photorespiration as a means of light protection have been extensively studied: “Plants that are impaired in their ability to carry out photorespiration (due to defective genes) are more susceptible to damage induced by excess light. Researchers consider this clear evidence that photorespiration acts to neutralize the otherwise damaging products of the light reactions, which build up when a low CO2 concentration limits the progress of the Calvin cycle. “(Campbell 2009). Despite initial intuition regarding the wasteful nature of photorespiration, closer analyses of the metabolic process uncovers the beneficial implications of RuBP+O2 in moderation.
Arriving at the end of my journey through the different facets of photorespiration, it is clear to see that amidst the detrimental impacts of an inherently wasteful metabolic process are glimmers of beneficial assets. The production of Glutathione, drought stress protection, plant “sunscreen”, etc. all affirm the premise that photorespiration does deserve to evolutionary exist and persist into the future. Hence the ultimate question and thesis of this blog appears to be answered: photorespiration survived despite its wasteful properties due to its protective properties (in moderation of course) against drought, free radicals, overexposure, etc. With that said, other questions still lurk beneath the surface. What is the threshold for photorespiration –exactly how much photorespiration is too much? Can photorespiration be genetically induced via biotechnology? If so, what are the economic and agricultural implications of genetically engineered photorespiration in regions of heavy droughts? Hopefully, these questions will be answered as research on photorespiration proliferates through the biological community, and as I trudge deeper into the topical literature. Until next time!
Explore these sources!
Astrid Wingler, Peter J. Lea, W. Paul Quick, and Richard C. Leegood, 2000. Photorespiration: metabolic pathways and their role in stress protection. Retrieved from http://eprints.whiterose.ac.uk/164/1/leegoodrc6.pdf
Jane B. Reece, Neil A Campbell, et.al. 2011. Campbell Biology. Pearson.
Catherine Gutherie , 2014. Glutathione: The Great Protector. Experience Life. Retrieved from <https://experiencelife.com/article/glutathione-the-great-protector/>.