Arctic marine forest distribution models showcase potentially severe habitat losses for cryophilic species under climate change.

The Arctic is among the fastest-warming areas of the globe. Understanding the impact of climate change on foundational Arctic marine species is needed to provide insight on ecological resilience at high latitudes. Marine forests, the underwater seascapes formed by seaweeds, are predicted to expand their ranges further north in the Arctic in a warmer climate. Here, we investigated whether northern habitat gains will compensate for losses at the southern range edge by modelling marine forest distributions according to three distribution categories: cryophilic (species restricted to the Arctic environment), cryotolerant (species with broad environmental preferences inclusive but not limited to the Arctic environment), and cryophobic (species restricted to temperate conditions) marine forests. Using stacked MaxEnt models, we predicted the current extent of suitable habitat for contemporary and future marine forests under Representative Concentration Pathway Scenarios of increasing emissions (2.6, 4.5, 6.0, and 8.5). Our analyses indicate that cryophilic marine forests are already ubiquitous in the north, and thus cannot expand their range under climate change, resulting in an overall loss of habitat due to severe southern range contractions. The extent of marine forests within the Arctic basin, however, is predicted to remain largely stable under climate change with notable exceptions in some areas, particularly in the Canadian Archipelago. Succession may occur where cryophilic and cryotolerant species are extirpated at their southern range edge, resulting in ecosystem shifts towards temperate regimes at mid to high latitudes, though many aspects of these shifts, such as total biomass and depth range, remain to be field validated. Our results provide the first global synthesis of predicted changes to pan-Arctic coastal marine forest ecosystems under climate change and suggest ecosystem transitions are unavoidable now for some areas.

Evidence for the introduction of the Asian red alga Neosiphonia japonica and its introgression with Neosiphonia harveyi (Ceramiales, Rhodophyta) in the Northwest Atlantic.

There is currently conflict in the literature on the taxonomic status of the reportedly cosmopolitan species Neosiphonia harveyi, a common red alga along the coast of Atlantic Canada and New England, USA. Neosiphonia harveyi sensu lato was assessed using three molecular markers: COI-5P, ITS and rbcL. All three markers clearly delimited three genetic species groups within N. harveyi sensu lato in this region, which we identified as N. harveyi, N. japonica and Polysiphonia akkeshiensis (here resurrected from synonymy with N. japonica). Although Neosiphonia harveyi is considered by some authors to be introduced to the Atlantic from the western Pacific, it was only confirmed from the North Atlantic suggesting it is native to this area. In contrast, Neosiphonia japonica was collected from only two sites in Rhode Island, USA, as well as from its reported native range in Asia (South Korea), which when combined with data in GenBank indicates that this species was introduced to the Northwest Atlantic. The GenBank data further indicate that N. japonica was also introduced to North Carolina, Spain, Australia and New Zealand. Despite the fact that all three markers clearly delimited N. harveyi and N. japonica as distinct genetic species groups, the ITS sequences for some N. harveyi individuals displayed mixed patterns and additivity indicating introgression of nuclear DNA from N. japonica into N. harveyi in the Northwest Atlantic. Introgression of DNA from an introduced species to a native species (i.e. 'genetic pollution') is one of the possible consequences of species introductions, and we believe this is the first documented evidence for this phenomenon in red algae.

Kelp forest community structure and demography in Kongsfjorden (Svalbard) across 25 years of Arctic warming.

The Arctic archipelago of Svalbard is a hotspot of global warming and many fjords experience a continuous increase in seawater temperature and glacial melt while sea-ice cover declines. In 1996/1998, 2012-2014, and 2021 macroalgal biomass and species diversity were quantified at the study site Hansneset, Kongsfjorden (W-Spitsbergen) in order to identify potential changes over time. In 2021, we repeated the earlier studies by stratified random sampling (1 × 1 m2, n = 3) along a sublittoral depth transect (0, 2.5, 5, 10, and 15 m) and investigated the lower depth limits of dominant brown algae between 3 and 19 m. The maximum fresh weight (FW) of all seaweeds was 11.5 kg m-2 at 2.5 m and to 99.9% constituted of kelp. Although biomass distribution along the depth transect in 2021 was not significantly different compared to 2012/2013, the digitate kelp community (Laminaria digitata/Hedophyllum nigripes) had transformed into an Alaria esculenta-dominated kelp forest. Consequently, a pronounced shift in kelp forest structure occurred over time as we demonstrate that biomass allocation to thallus parts is kelp species-specific. Over the past decade, kelp demography changed and in 2021 a balanced age structure of kelps (juveniles plus many older kelp individuals) was only apparent at 2.5 m. In addition, the abundances and lower depth limits of all dominant brown algae declined noticeably over the last 25 years while the red algal flora abundance remained unchanged at depth. We propose that the major factor driving the observed changes in the macroalgal community are alterations in underwater light climate, as in situ data showed increasing turbidity and decreasing irradiance since 2012 and 2017, respectively. As a consequence, the interplay between kelp forest retreat to lower depth levels caused by coastal darkening and potential macroalgal biomass gain with increasing temperatures will possibly intensify in the future with unforeseen consequences for melting Arctic coasts and fjord ecosystem services.

Defining regulatory regions in the rat prolactin gene family locus using a large P1 genomic clone.

Members of the large rat prolactin gene family located on chromosome 17 are expressed in one or more placental trophoblast cell types and maternal decidua at specific times during pregnancy. Studies to identify the factors involved in these highly specific developmental expression patterns, using limited amounts of 5'-flanking DNA, have met with only partial success. Here we report the isolation and characterization of an 80-kb rat genomic clone, P1 12830, containing linked rat placental lactogen II, rat prolactin-like protein-I, and rat prolactin-like protein-B genes with substantial amounts of 5'- and 3'-flanking DNA as well as a rat placental lactogen II-related pseudogene, the first to be described in this gene family. This clone was used to create F0 transgenic mice, and the levels of expression of the three rat genes were compared with those of the endogenous mouse genes, using RT-PCR. Each rat gene was expressed differently in the same placenta, confirming the importance of sufficient flanking sequences in the expression of the individual genes. These studies emphasize the need for large genomic clones in defining the complete complement of factors that regulate the developmental expression of the rat prolactin gene locus.

U-46619 but not serotonin increases endocannabinoid content in middle cerebral artery: evidence for functional relevance.

Cerebral vascular smooth muscle cells express the CB(1) cannabinoid receptor, and CB(1) receptor agonists produce vasodilation of cerebral arteries. The purpose of this study was to determine whether vasoconstriction of rat middle cerebral artery (MCA) results in the local formation of endocannabinoids (eCBs), which, via activation of CB(1) receptors, oppose the vasoconstriction in a feedback manner. The thromboxane A(2) (TXA(2)) mimetic U-46619 significantly increased N-arachidonylethanolamine (AEA) and 2-arachidonylglycerol (2-AG) content of isolated MCA, whereas 5-hydroxytrypamine (5-HT) decreased AEA and 2-AG content. If eCBs play a feedback role in the regulation of MCA tone, then CB(1) receptor antagonists should enhance the constriction of MCA produced by U-46619 but not 5-HT. U-46619 caused concentration-dependent constrictions of endothelium-denuded MCA. Two CB(1) receptor antagonists SR-141716 and AM-251 decreased the EC(50) value for U-46619 to constrict endothelium-denuded MCA without affecting the maximal effect. A low concentration of CB(1) receptor agonist Win-55212-2 (30 nM) produced vasodilation of MCAs constricted with low but not saturating concentrations of U-46619. SR-141716 had no effect on the 5-HT concentration-contraction relationship. These data suggest that TXA(2) receptor activation increases MCA eCB content, which, via activation of CB(1) receptors, reduces the constriction produced by moderate concentrations of the TXA(2) agonist. Although 5-HT-induced vasoconstriction is reduced by exogenous CB(1) receptor agonist, activation of 5-HT receptors does not increase eCB content. These results suggest that MCA production of eCBs is not regulated by constriction per se but likely via a signaling pathway that is specific for TXA(2) receptors and not 5-HT receptors.

Genotyping and phenotyping of beta2-toxigenic Clostridium perfringens fecal isolates associated with gastrointestinal diseases in piglets.

Although Clostridium perfringens is recognized as an important cause of clostridial enteric diseases, only limited knowledge exists concerning the association of particular C. perfringens toxinotypes (type A to E) with gastrointestinal (GI) diseases in domestic animals. Some C. perfringens isolates also produce the newly discovered beta2-toxin (CPB2). Recent epidemiological studies suggested that C. perfringens isolates carrying the gene encoding CPB2 (cpb2) are strongly associated with clostridial GI diseases in domestic animals, including necrotic enteritis in piglets and typhlocolitis in horses. These putative relationships, obtained by PCR genotyping, were tested in the present study by further genotyping and phenotyping of 29 cpb2-positive C. perfringens isolates from pigs with GI disease (pig GI disease isolates). PCR and restriction fragment length polymorphism analysis reconfirmed the presence of cpb2 gene sequences in all the disease isolates included in the study. Furthermore, genotyping by pulsed-field gel electrophoresis analyses showed that the pig GI disease isolates included in this study all carry a plasmid cpb2 gene, yet no clonal relationships were detected between the cpb2-positive pig GI disease isolates surveyed. Finally, CPB2-specific Western blotting demonstrated CPB2 expression by all of the cpb2-positive isolates surveyed. The CPB2 proteins made by five of these pig GI disease isolates were shown to have the same deduced amino acid sequences as the biologically active CPB2 protein made by the original type C isolate, CWC245. Collectively, our present results support a significant association between CPB2-positive C. perfringens isolates and diarrhea in piglets.