A method of identifying microorganisms with reduced adaptability to a particular environment, wherein (1) each microorganism is independent by insertional inactivation of a gene with a nucleic acid comprising a unique marker sequence. Mutating to provide a plurality of microorganisms, or clones of said microorganisms, such that each mutation has a different label sequence; (2) providing storage samples of each mutation produced by step (1), respectively, and providing storage nucleic acids each comprising a unique label sequence from each mutation; (3) introducing a plurality of mutations produced by step (1) into the specific environment such that the microorganisms capable of growing in the specific environment grow in the above environment; (4) recovering the microorganisms or selected portions thereof from the environment and separating nucleic acids from the recovered microorganisms; (5) comparing all label sequences in the nucleic acid isolated in step (4) with the unique label sequences of each of the stored mutations as in step (2); and (6) any label isolated in step (4). Screening for individual mutations that also do not have a sequence.

Identification of genes

Shifts in vegetation phenology are a key example of the biological effects of climate change1–3. However, there is substantial uncertainty about whether these temperature-driven trends will continue, or whether other factors—for example, photoperiod—will become more important as warming exceeds the bounds of historical variability4,5. Here we use phenological transition dates derived from digital repeat photography6 to show that experimental whole-ecosystem warming treatments7 of up to +9 °C linearly correlate with a delayed autumn green-down and advanced spring green-up of the dominant woody species in a boreal Picea–Sphagnum bog. Results were confirmed by direct observation of both vegetative and reproductive phenology of these and other bog plant species, and by multiple years of observations. There was little evidence that the observed responses were constrained by photoperiod. Our results indicate a likely extension of the period of vegetation activity by 1–2 weeks under a ‘CO2 stabilization’ climate scenario (+2.6 ± 0.7 °C), and 3–6 weeks under a ‘high-CO2 emission’ scenario (+5.9 ± 1.1 °C), by the end of the twenty-first century. We also observed severe tissue mortality in the warmest enclosures after a severe spring frost event. Failure to cue to photoperiod resulted in precocious green-up and a premature loss of frost hardiness8, which suggests that vulnerability to spring frost damage will increase in a warmer world9,10. Vegetation strategies that have evolved to balance tradeoffs associated with phenological temperature tracking may be optimal under historical climates, but these strategies may not be optimized for future climate regimes. These in situ experimental results are of particular importance because boreal forests have both a circumpolar distribution and a key role in the global carbon cycle11. Experimental whole-ecosystem warming treatments of a Picea–Sphagnum peat bog reveal the likely phenological consequences of future temperature increases that exceed those of historical climate regimes.

Ecosystem warming extends vegetation activity but heightens vulnerability to cold temperatures

In temperate and boreal ecosystems, seasonal cycles of growth and dormancy allow perennial plants to adapt to winter conditions. We show, in hybrid aspen trees, that photoperiodic regulation of dormancy is mechanistically distinct from autumnal growth cessation. Dormancy sets in when symplastic intercellular communication through plasmodesmata is blocked by a process dependent on the phytohormone abscisic acid. The communication blockage prevents growth-promoting signals from accessing the meristem. Thus, precocious growth is disallowed during dormancy. The dormant period, which supports robust survival of the aspen tree in winter, is due to loss of access to growth-promoting signals.

http://science.sciencemag.org/content/sci/360/6385/212.full.pdf

Photoperiodic control of seasonal growth is mediated by ABA acting on cell-cell communication

Accurate predictions of spring plant phenology with climate change are critical for projections of growing seasons, plant communities and a number of ecosystem services, including carbon storage. Progress towards prediction, however, has been slow because the major cues known to drive phenology - temperature (including winter chilling and spring forcing) and photoperiod - generally covary in nature and may interact, making accurate predictions of plant responses to climate change complex and nonlinear. Alternatively, recent work suggests many species may be dominated by one cue, which would make predictions much simpler. Here, we manipulated all three cues across 28 woody species from two North American forests. All species responded to all cues examined. Chilling exerted a strong effect, especially on budburst (-15.8 d), with responses to forcing and photoperiod greatest for leafout (-19.1 and -11.2 d, respectively). Interactions between chilling and forcing suggest that each cue may compensate somewhat for the other. Cues varied across species, leading to staggered leafout within each community and supporting the idea that phenology is a critical aspect of species' temporal niches. Our results suggest that predicting the spring phenology of communities will be difficult, as all species we studied could have complex, nonlinear responses to future warming.

https://nph.onlinelibrary.wiley.com/doi/pdf/10.1111/nph.15232

Temperature and photoperiod drive spring phenology across all species in a temperate forest community

Phenology is a key aspect of plant and animal life strategies that determines the ability to capture seasonally variable resources. It defines the season and duration of growth and reproduction and paces ecological interactions and ecosystem functions. Phenology models have become a key component of models in agronomy, forestry, ecology, and biogeosciences. Plant and animal process-based phenology models have taken different paths that have so far not crossed. Yet, they share many features because plant and animal annual cycles also share many characteristics, from their stepwise progression, including a resting period, to their dependence on similar environmental factors. We review the strengths and shortcomings of these models and the divergences in modeling approaches for plants and animals, which are mostly due to specificities of the questions they tackle. Finally, we discuss the most promising avenues and the challenges phenology modeling needs to address in the upcoming years.

Process-Based Models of Phenology for Plants and Animals

Contents 511 I. 511 II. 512 III. 513 IV. 513 V. 517 VI. 517 VII. 521 VIII. 521 Acknowledgements 521 References 521 SUMMARY: Trees growing in boreal and temperate regions synchronize their growth with seasonal climatic changes in adaptive responses that are essential for their survival. These trees cease growth before the winter and establish a dormant state during which growth cessation is maintained by repression of responses to growth-promotive signals. Reactivation of growth in the spring follows the release from dormancy promoted by prolonged exposure to low temperature during the winter. The timing of the key events and regulation of the molecular programs associated with the key stages of the annual growth cycle are controlled by two main environmental cues: photoperiod and temperature. Recently, key components mediating photoperiodic control of growth cessation and bud set have been identified, and striking similarities have been observed in signaling pathways controlling growth cessation in trees and floral transition in Arabidopsis. Although less well understood, the regulation of bud dormancy and bud burst may involve cell-cell communication and chromatin remodeling. Here, we discuss current knowledge of the molecular-level regulation of the annual growth cycle of woody trees in temperate and boreal regions, and identify key questions that need to be addressed in the future.

Photoperiod- and temperature-mediated control of phenology in trees – a molecular perspective

The effects of Arabic gum (AG) against nephrotoxicity of mercury (Hg), an oxidative-stress inducing substance, in rats were investigated. A single dose of mercuric chloride (5 mg/kg intraperitoneal injection) induced renal toxicity, manifested biochemically by a significant increase in serum creatinine, blood urea nitrogen, thiobarbituric acid reactive substances, and total nitrate/nitrite production in kidney tissues. In addition, reduced glutathione, glutathione peroxidase, and catalase enzymes in renal tissues were significantly decreased. Pretreatment of rats with AG (7.5 g/kg/day per oral administration), starting 5 days before mercuric chloride injection and continuing through the experimental period, resulted in a complete reversal of Hg-induced increase in creatinine, blood urea nitrogen, thiobarbituric acid reactive substances, and total nitrate/nitrite to control values. Histopathologic examination of kidney tissues confirmed the biochemical data; pretreatment of AG prevented Hg-induced degenerative changes of kidney tissues. These results indicate that AG is an efficient cytoprotective agent against Hg-induced nephrotoxicity by a mechanism related at least in part to its ability to decrease oxidative and nitrosative stress and preserve the activity of antioxidant enzymes in kidney tissues.

/pdf/antioxidant-effect-of-arabic-gum-against-mercuric-chloride-4ql8og6izo.pdf

Antioxidant effect of Arabic gum against mercuric chloride-induced nephrotoxicity.

Blood chemical changes and renal histological alterations induced by gentamicin in rats.

Background Kidney is a vital organ which plays an important and irreplaceable role in detoxification and removal of xenobiotics. And therefore is vulnerable to develop various forms of injuries. Hence, making it immensely important to search for natural reno-protective compounds. Objectives This study therefore, aims to evaluate the reno-protective properties of propolis against gentamicin induced renal toxicity in mice. Methods Three groups of 10 male mice each were used for this study. First group served as control, the second group (Gm group) was administered orally 80 mg/kg body weight gentamicin for 7 days, and the third group (GmP group) was administered same dose of gentamicin with propolis (500 mg/kg body weight) for 7 days. Various parameters were used to study the renal toxicity. Results Gentamicin caused significant renal damage as evident by the rise in BUN levels, diminished glomeruli hypocellularity, moderately dilated tubules, and mild loss of brush border, severe infiltration, extensive tubular degeneration and presence of tubular cast. Histochemistry results show presence of collagen and reticular fibres. Immunohistochemical reactions show kidney injury (Kim-1 gene-expression), oxidative stress (MDA gene-expression), and an increase in apoptosis (caspase-3 gene-expression). Co-administration of propolis with gentamicin showed significant decrease in BUN levels, appearance of healthy glomeruli with normal cellularity, reduction of tubular injury, decrease of collagen and reticular fibres deposition, reduction of apoptosis, kidney injury and oxidative stress. Conclusion Results presented in this study clearly show the reno-protective role of propolis against gentamicin-induced toxicity on mice kidney.

http://scielo.isciii.es/pdf/nefrologia/v36n6/0211-6995-nefrologia-36-06-00643.pdf

Reno-protective effects of propolis on gentamicin-induced acute renal toxicity in swiss albino mice

http://fac.ksu.edu.sa/sites/default/files/attenuation_pdf.pdf

Badr Aldahmash

Papers

Photoperiod- and temperature-mediated control of phenology in trees – a molecular perspective

Antioxidant effect of Arabic gum against mercuric chloride-induced nephrotoxicity.

Blood chemical changes and renal histological alterations induced by gentamicin in rats.

Reno-protective effects of propolis on gentamicin-induced acute renal toxicity in swiss albino mice

Attenuation of hepatotoxicity and oxidative stress in diabetes STZ-induced type 1 by biotin in Swiss albino mice