230 research outputs found
3a,11b-Dihydroxy-2-oxo-2,3,3a,11b-tetrahydro-1H-imidazo[4,5-f][1,10]phenanthrolin-7-ium chloride
In the crystal structure of the title compound, C13H11N4O3
+·Cl−, the dihedral angle between the two pyridine rings is 9.72 (9) Å. Ions are linked via N—H⋯Cl, O—H⋯Cl and O—H⋯O hydrogen bonds, forming a three-dimensional framework
Demographic and net primary productivity dynamics of primary and secondary tropical forests in Southwest China under a changing climate
Tropical forests are major carbon sinks on the Earth's land surface. However, our understanding of how the demographic rate and carbon sink capacities of tropical forests respond to climate change remains limited. In this study, we investigated the impacts of environmental drivers on forest growth, mortality, recruitment, and stem net primary productivity (NPPstem) over 16 years at five tropical forest plots in Xishuangbanna, Southwest China. These plots are along a successional gradient spanning three tropical secondary forests (tropical secondary forest‐1 [TSF‐1], tropical secondary forest‐2 [TSF‐2], and tropical secondary forest‐3 [TSF‐3]) and two primary forests (tropical rainforest [TRF] and tropical karst forest [TKF]). Our results showed that early successional secondary forests (TSF‐2 and TSF‐3) had higher diameter growth rates and relative mortality rates. An extreme drought event during 2009–2010 reduced the growth rate, relative recruitment rate, and NPPstem for most plots while increasing mortality in early successional forest plots. We observed significant negative effects of maximum temperature (Tmax) on NPPstem and diameter growth rate across all plots. Additionally, we found that precipitation had significant positive effects on diameter growth rate across all plots. Furthermore, tree mortality increased with rising Tmax, whereas precipitation significantly enhanced tree recruitment. Our findings highlight the vulnerability of tree growth, mortality, recruitment, and productivity in tropical forests to extreme drought events in Southwest China. Continued climate warming and more frequent droughts will induce higher mortality rates and impede growth, thus reducing the carbon sink capacity of tropical forests, especially in early successional stage tropical secondary forests
2-(2-Furyl)-1H-imidazo[4,5-f][1,10]phenanthroline-3,7-diium dichloride monohydrate
The organic cation of the title salt, C17H12N4O2+·2Cl−·H2O, is nearly planar, the dihedral angle between two pyridine rings being 2.53 (16)° and that between the pyridinum and furan rings being 4.17 (19)°. Molecules are linked via N—H⋯O, N—H⋯Cl and O—H⋯Cl hydrogen bonds, forming a three-dimensional framework and π–π stacking interactions help to stabilize the crystal structure [the imidazole–pyridine and imidazole–benzene centroid–centroid distances are 3.501 (3) and 3.674 (3) Å; respectively]
Calcium-sensing receptor regulates stomatal closure through hydrogen peroxide and nitric oxide in response to extracellular calcium in Arabidopsis
The Arabidopsis calcium-sensing receptor CAS is a crucial regulator of extracellular calcium-induced stomatal closure. Free cytosolic Ca2+ (Ca2+i) increases in response to a high extracellular calcium (Ca2+o) level through a CAS signalling pathway and finally leads to stomatal closure. Multidisciplinary approaches including histochemical, pharmacological, fluorescent, electrochemical, and molecular biological methods were used to discuss the relationship of hydrogen peroxide (H2O2) and nitric oxide (NO) signalling in the CAS signalling pathway in guard cells in response to Ca2+o. Here it is shown that Ca2+o could induce H2O2 and NO production from guard cells but only H2O2 from chloroplasts, leading to stomatal closure. In addition, the CASas mutant, the atrbohD/F double mutant, and the Atnoa1 mutant were all insensitive to Ca2+o-stimulated stomatal closure, as well as H2O2 and NO elevation in the case of CASas. Furthermore, it was found that the antioxidant system might function as a mediator in Ca2+o and H2O2 signalling in guard cells. The results suggest a hypothetical model whereby Ca2+o induces H2O2 and NO accumulation in guard cells through the CAS signalling pathway, which further triggers Ca2+i transients and finally stomatal closure. The possible cross-talk of Ca2+o and abscisic acid signalling as well as the antioxidant system are discussed
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