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MacLeod, R.

Publications and source records attributed to MacLeod, R..

3 recordsLinked to original sources

Immediate methane and carbon dioxide release from exposed permafrost at an active retrogressive thaw slump in the Canadian Arctic

The Arctic is warming rapidly, causing permafrost thaw and accelerating the release of greenhouse gases. Rapid thaw features such as retrogressive thaw slumps are increasing in frequency and severity across the Arctic; however, their associated greenhouse gas emissions are poorly constrained. Current estimates of emissions from retrogressive thaw slumps rely largely on laboratory incubations and carbon stock estimates rather than in-situ field measurements. Here we directly quantify methane and carbon dioxide fluxes from the exposed headwall of an active retrogressive thaw slump. We show that thaw immediately releases biogenic methane and carbon dioxide, originating from gases trapped within the frozen soil matrix. Microbial transcription of methyl-coenzyme M reductase suggests archaea carrying out methanogenesis at subzero temperatures are the source of trapped methane. Carbon emissions varied by an order of magnitude among cryostratigraphic units, reflecting differences in geomorphologic history, organic carbon and nitrogen content, and microbial community composition. Carbon emissions were highest from organic-rich paleo cryosols from the Late Holocene that contained abundant methanogenic archaea. We estimate that [~]300 kg C (CO2 equivalents) is emitted annually from the headwall of this small thaw slump (surface area of [~]1200 m2). Considering the thousands of active slumps and extensive coastal permafrost erosion across the northern continuous permafrost zone, such features may represent a growing natural source of GHG emissions. These findings indicate that current permafrost carbon feedback models underestimate GHG release by omitting the direct release of trapped gases stored in permafrost.

ecology↗

A Novel Approach for Using Thermal Imaging to Study Behavioural Responses to Environmental Stressors in Passerines

Infrared thermography is a promising tool for assessing proxy for stress response in animals. With the advancement of longer recording capabilities, this technique allows the monitoring of the dynamic nature of the temperature variation which is highly correlated to the stress faced by the animal. The current method of extraction of data from thermal videos involves manual identification of the beginning and end of the activity (feeding bout in our case) and extracting the temperature data into CSV files. In this paper, we aim to identify the beginning and ending of the feeding bout by the Identification of Temperature Change (ITC) that happens when a bird arrives and leaves the frame. By identifying this we can monitor longer IRT videos and extract the thermal imaging data for stress monitoring in a faster manner. The identification of the beginning and end frames, also allows us to get behavioural data such as feeding bout length and feeding frequency which also act as a proxy for perceived stress. This method was developed to simplify the data analysis process of thermal imaging videos and proved to be an effective method with wider applications in behavioural monitoring based on temperature change.

animal behavior and cognition↗

Phosphodiesterase Type 4 anchoring regulates cAMP signaling to Popeye domain-containing proteins.

Cyclic AMP is a ubiquitous second messenger used to transduce intracellular signals from a variety of Gs-coupled receptors. Compartmentalisation of protein intermediates within the cAMP signaling pathway underpins receptor-specific responses. The cAMP effector proteins protein-kinase A and EPAC are found in complexes that also contain phosphodiesterases whose presence ensures a coordinated cellular response to receptor activation events. Popeye proteins are the most recent class of cAMP effectors to be identified and have crucial roles in cardiac pacemaking and conduction. We report the first observation that Popeye proteins exist in complexes with members of the PDE4 family in cardiac myocytes thus restricting cAMP signaling. We show that POPDC1 preferentially binds the PDE4A sub-family via a specificity motif in the PDE4 UCR1 region and that PDE4s bind to the Popeye domain of POPDC1 in a region known to be susceptible to a mutation that causes human disease. Using a cell-permeable disruptor peptide that displaces the POPDC1-PDE4 complex we show that PDE4 activity localized to POPDC1 is essential to maintain action potential duration in beating cardiac myocytes.

biochemistry↗