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Increasing water scarcity and rapid socio-economic development are driving farmers in Asia to transform traditionally flooded rice cropping systems into non-flooded crop production. The management of earthworms in non-flooded rice fields appears to be a promising strategy to support residue recycling and mitigate greenhouse gas (GHG) emissions triggered by residue amendment. We conducted a field experiment on non-flooded rainfed rice fields, with and without residue amendment. In-situ mesocosms were inoculated with endogeic earthworms (Metaphire sp.), with either low (ET1: 150 individuals m - 2 ), or high density (ET2: 450 individuals m - 2 ), and a control (ET0: no earthworms). We measured GHG emissions (methane (CH 4 ); nitrous oxide (N 2 O); carbon dioxide (CO 2 )) twice a week during the cropping season with static chambers. Effects of earthworms on yield and root growth were additionally assessed. Earthworms offset the enormous increase of CH 4 emissions induced by straw amendment (from 4.6 ± 5 to 75.3 ± 46 kg CH 4 -C ha - 1 in ET0). Earthworm activity significantly reduced CH 4 release, particularly at ET2, by more than one-third (to 22 ± 15 kg CH 4 -C ha - 1 ). In contrast, earthworm inoculation did not affect N 2 O emission. Straw amendment more than doubled the global warming potential (GWP). Earthworms reduced GWP by 39% at low (ET1) and 55% at high densities (ET2). Earthworm activity reduced root mass density under conditions of straw amendment but did not affect yield. Earthworms can significantly reduce detrimental effects of rice crop residue amendment on GHG release under upland rice production. Organic carbon (C) might be preserved in earthworm casts and thereby limit C availability for CH 4 production. At the same time, earthworm activity might increase methanotrophic CH 4 consumption, due to improved soil aeration or less root exudates. Consequently, earthworms have a strong potential for regulating ecosystem functions related to rice straw decomposition, nutrient allocation and thus GHG reduction., Competing Interests: Declaration of competing interest All authors have participated in conception and design, or analysis and interpretation of the data; drafting the article or revising it critically for important intellectual content; and approval of the final version. This manuscript has not been submitted to, nor is under review at, another journal or other publishing venue. The authors have no affiliation with any organization with a direct or indirect financial interest in the subject matter discussed in the manuscript., (Copyright © 2018 Elsevier B.V. All rights reserved.)

The NAD-glycohydrolase/ADP-ribosyl cyclase CD38 catalyzes the metabolism of nicotinamide adenine dinucleotide (NAD) to the Ca 2+ mobilizing second messengers ADP-ribose (ADPR), 2'-deoxy-ADPR, and cyclic ADP-ribose (cADPR). In the present study, we investigated binding and metabolism of NAD by a soluble fragment of human CD38, sCD38, and its catalytically inactive mutant by monitoring changes in endogenous tryptophan (Trp) fluorescence. Addition of NAD resulted in a concentration-dependent decrease in sCD38 fluorescence that is mainly caused by the Trp residue W189. Amplitude of the fluorescence decrease was fitted as one-site binding curve revealing a dissociation constant for NAD of 29 μM. A comparable dissociation constant was found with the catalytically inactive sCD38 mutant (K D 37 μM NAD) indicating that binding of NAD is not significantly affected by the mutation. The NAD-induced decrease in Trp fluorescence completely recovered in case of sCD38. Kinetics of recovery was slowed down with decreasing temperature and sCD38 concentration and increasing NAD concentration demonstrating that recovery in fluorescence is proportional to the enzymatic activity of sCD38. Accordingly, recovery in fluorescence was not observed with the catalytically inactive mutant. This article is part of a Special Issue entitled: ECS Meeting edited by Claus Heizmann, Joachim Krebs and Jacques Haiech., (Copyright © 2018 Elsevier B.V. All rights reserved.)

G protein coupled receptors regulate numerous cellular functions primarily via coupling to heterotrimeric G proteins and subsequent regulation of effector proteins such as ion channels, enzymes or GTP exchange factors for small G proteins. The dynamics of interactions between G protein subunits and effectors have been difficult to study particularly in a cellular context. The introduction of Förster resonance energy transfer methods into the field of GPCR research led to interesting insights into the temporal patterns of interactions between G protein subunits and their effectors. In this review we specifically focus on the interaction of Gαi subunits with adenylyl cyclases and of Gαq subunits with p63RhoGEF or G protein coupled receptor kinases type 2. Comparing the dynamics of these interactions revealed remarkable differences between different G protein effectors regarding the ability to be modulated by members of the regulator of G protein signalling protein family as well as the sensitivity towards receptor activation., (Copyright © 2015 Elsevier GmbH. All rights reserved.)