Dimethyl Disulfide Produced by the Naturally Associated Bacterium Bacillus sp B55 Promotes Nicotiana attenuata Growth by Enhancing Sulfur Nutrition

Bacillus sp B55, a bacterium naturally associated with Nicotiana attenuata roots, promotes growth and survival of wild-type and, particularly, ethylene (ET)–insensitive 35S-ethylene response1 (etr1) N. attenuata plants, which heterologously express the mutant Arabidopsis thaliana receptor ETR1-1. We found that the volatile organic compound (VOC) blend emitted by B55 promotes seedling growth, which is dominated by the S-containing compound dimethyl disulfide (DMDS). DMDS was depleted from the headspace during cocultivation with seedlings in bipartite Petri dishes, and ³⁵S was assimilated from the bacterial VOC bouquet and incorporated into plant proteins. In wild-type and 35S-etr1 seedlings grown under different sulfate (SO₄⁻²) supply conditions, exposure to synthetic DMDS led to genotype-dependent plant growth promotion effects. For the wild type, only S-starved seedlings benefited from DMDS exposure. By contrast, growth of 35S-etr1 seedlings, which we demonstrate to have an unregulated S metabolism, increased at all SO₄⁻² supply rates. Exposure to B55 VOCs and DMDS rescued many of the growth phenotypes exhibited by ET-insensitive plants, including the lack of root hairs, poor lateral root growth, and low chlorophyll content. DMDS supplementation significantly reduced the expression of S assimilation genes, as well as Met biosynthesis and recycling. We conclude that DMDS by B55 production is a plant growth promotion mechanism that likely enhances the availability of reduced S, which is particularly beneficial for wild-type plants growing in S-deficient soils and for 35S-etr1 plants due to their impaired S uptake/assimilation/metabolism.     

The Tetrapod Ichnogenus Protochirotherium Fichter and Kunz 2004, a Characteristic Early Triassic Morphotype of Central Pangea

Early Triassic chirotherian footprint assemblages from Poland, Germany, and Morocco are important for understanding archosaur evolution in the aftermath of the Permian-Triassic crisis. However, their ichnotaxonomy is confusing because various authors have interpreted their diversity differently. After an analysis and ichnotaxonomic re-assessment, the presence of the ichnogenera Brachychirotherium, Isochirotherium, and Chirotherium in these assemblages is not supported. Distant similarities with these ichnotaxa are functions of extra morphological variation and substrate-related factors. Instead, Early Triassic chirotherian footprints described under these names are assigned here to the ichnogenus Protochirotherium and to a more slender morphotype identified as Synaptichnium. In particular, Protochirotherium appears to be more widely distributed in central Pangea as a characteristic morphotype reflecting a distinct stage in archosaur evolution. Trackmakers were nonarchosaurian archosauriforms or, alternatively, stem-group crocodylians. Morphologically and temporally these footprints match the hypothetical ancestor of the Chirotherium barthii trackmaker. Chirotherium barthii appears by the beginning of the Middle Triassic. Because of its restricted stratigraphic range, and its wider distribution in central Pangea, Protochirotherium also has biostratigraphic significance for this region and can be considered as an indicator of Early Triassic-aged strata.     

Cholesterol accumulation caused by low density lipoprotein receptor deficiency or a cholesterol-rich diet results in ectopic bone formation during experimental osteoarthritis

Introduction

Osteoarthritis (OA) is associated with the metabolic syndrome, however the underlying mechanisms remain unclear. We investigated whether low density lipoprotein (LDL) accumulation leads to increased LDL uptake by synovial macrophages and affects synovial activation, cartilage destruction and enthesophyte/osteophyte formation during experimental OA in mice.

Methods

LDL receptor deficient (LDLr^−/−) mice and wild type (WT) controls received a cholesterol-rich or control diet for 120 days. Experimental OA was induced by intra-articular injection of collagenase twelve weeks after start of the diet. OA knee joints and synovial wash-outs were analyzed for OA-related changes. Murine bone marrow derived macrophages were stimulated with oxidized LDL (oxLDL), whereupon growth factor presence and gene expression were analyzed.

Results

A cholesterol-rich diet increased apolipoprotein B (ApoB) accumulation in synovial macrophages. Although increased LDL levels did not enhance thickening of the synovial lining, S100A8 expression within macrophages was increased in WT mice after receiving a cholesterol-rich diet, reflecting an elevated activation status. Both a cholesterol-rich diet and LDLr deficiency had no effect on cartilage damage; in contrast, ectopic bone formation was increased within joint ligaments (fold increase 6.7 and 6.1, respectively). Moreover, increased osteophyte size was found at the margins of the tibial plateau (4.4 fold increase after a cholesterol-rich diet and 5.3 fold increase in LDLr^−/− mice). Synovial wash-outs of LDLr^−/− mice and supernatants of macrophages stimulated with oxLDL led to increased transforming growth factor-beta (TGF-β) signaling compared to controls.

Conclusions

LDL accumulation within synovial lining cells leads to increased activation of synovium and osteophyte formation in experimental OA. OxLDL uptake by macrophages activates growth factors of the TGF-superfamily.     

Brown adipose tissue functions in humans

Human adults have functionally active BAT. The metabolic function can be reliably measured in vivo using modern imaging modalities (namely PET/CT). Cold seems to be one of the most potent stimulators of BAT metabolic activity but other stimulators (for example insulin) are actively studied. Obesity is related to lower metabolic activity of BAT but it may be reversed after successful weight reduction such as after bariatric surgery. This article is part of a Special Issue entitled Brown and White Fat: From Signaling to Disease.     

Conserving Europe’s most endangered butterfly: the Macedonian Grayling (Pseudochazara cingovskii)

The Macedonian Grayling is listed as critically endangered in the recent IUCN Red List of European butterflies because of its extreme rarity and habitat loss due to quarrying. This categorisation was, however, based on rather limited knowledge on its actual distribution, population size and habitat requirements. In 2012, we conducted field surveys to acquire more information. We found the species at six new sites extending its known range of suitable habitat to just under 10 km². The daily population size was estimated using capture-mark-recapture method in the most densely populated part of the Pletvar pass site at more than 650 individuals. Adults proved to be extremely sedentary, not moving far even within the continuous habitat on the same slope. Oviposition was observed on dry plant material and in a rock crevice close to the potential larval host plant Festuca sp. Quarrying is confirmed to be the main threat to the habitat of the Macedonian Grayling with five out of seven populated sites containing active marble quarries. Due to the enlargement of the known area of occupancy, its threat status would now be estimated at endangered. Despite the restricted knowledge about its distribution and trends in the population size, the IUCN criteria proved to be applicable to determine the threat status of a rare and localized butterfly such as Pseudochazara cingovskii. Its original assessment of being called the most threatened butterfly in Europe resulted in immediate research project and subsequent actions that will undoubtedly help to conserve it in the future.     

Remodeling and spacing factor 1 (RSF1) deposits centromere proteins at DNA double-strand breaks to promote non-homologous end-joining

The cellular response to ionizing radiation (IR)-induced DNA double-strand breaks (DSBs) in native chromatin requires a tight coordination between the activities of DNA repair machineries and factors that modulate chromatin structure. SMARCA5 is an ATPase of the SNF2 family of chromatin remodeling factors that has recently been implicated in the DSB response. It forms distinct chromatin remodeling complexes with several non-canonical subunits, including the remodeling and spacing factor 1 (RSF1) protein. Despite the fact that RSF1 is often overexpressed in tumors and linked to tumorigenesis and genome instability, its role in the DSB response remains largely unclear. Here we show that RSF1 accumulates at DSB sites and protects human cells against IR-induced DSBs by promoting repair of these lesions through homologous recombination (HR) and non-homologous end-joining (NHEJ). Although SMARCA5 regulates the RNF168-dependent ubiquitin response that targets BRCA1 to DSBs, we found RSF1 to be dispensable for this process. Conversely, we found that RSF1 facilitates the assembly of centromere proteins CENP-S and CENP-X at sites of DNA damage, while SMARCA5 was not required for these events. Mechanistically, we uncovered that CENP-S and CENP-X, upon their incorporation by RSF1, promote assembly of the NHEJ factor XRCC4 at damaged chromatin. In contrast, CENP-S and CENP-X were dispensable for HR, suggesting that RSF1 regulates HR independently of these centromere proteins. Our findings reveal distinct functions of RSF1 in the 2 major pathways of DSB repair and explain how RSF1, through the loading of centromere proteins and XRCC4 at DSBs, promotes repair by non-homologous end-joining.     

Neural networks in intestinal immunoregulation

Key physiological functions of the intestine are governed by nerves and neurotransmitters. This complex control relies on two neuronal systems: an extrinsic innervation supplied by the two branches of the autonomic nervous system and an intrinsic innervation provided by the enteric nervous system. As a result of constant exposure to commensal and pathogenic microflora, the intestine developed a tightly regulated immune system. In this review, we cover the current knowledge on the interactions between the gut innervation and the intestinal immune system. The relations between extrinsic and intrinsic neuronal inputs are highlighted with regards to the intestinal immune response. Moreover, we discuss the latest findings on mechanisms underlying inflammatory neural reflexes and examine their relevance in the context of the intestinal inflammation. Finally, we discuss some of the recent data on the identification of the gut microbiota as an emerging player influencing the brain function.     

The effect of tissue-engineered cartilage biomechanical and biochemical properties on its post-implantation mechanical behavior

The insufficient load-bearing capacity of today’s tissue-engineered (TE) cartilage limits its clinical application. Focus has been on engineering cartilage with enhanced mechanical stiffness by reproducing native biochemical compositions. More recently, depth dependency of the biochemical content and the collagen network architecture has gained interest. However, it is unknown whether the mechanical performance of TE cartilage would benefit more from higher content of biochemical compositions or from achieving an appropriate collagen organization. Furthermore, the relative synthesis rate of collagen and proteoglycans during the TE process may affect implant performance. Such insights would assist tissue engineers to focus on those aspects that are most important. The aim of the present study is therefore to elucidate the relative importance of implant ground substance stiffness, collagen content, and collagen architecture of the implant, as well as the synthesis rate of the biochemical constituents for the post-implantation mechanical behavior of the implant. We approach this by computing the post-implantation mechanical conditions using a composition-based fibril-reinforced poro-viscoelastic swelling model of the medial tibia plateau. Results show that adverse implant composition and ultrastructure may lead to post-implantation excessive mechanical loads, with collagen orientation being the most critical variable. In addition, we predict that a faster synthesis rate of proteoglycans compared to that of collagen during TE culture may result in excessive loads on collagen fibers post-implantation. This indicates that even with similar final contents, constructs may behave differently depending on their development. Considering these aspects may help to engineer TE cartilage implants with improved survival rates.