Climate change and seasonal reproduction in mammals

Seasonal reproduction is common among mammals at all latitudes, even in the deep tropics. This paper (i) discusses the neuroendocrine pathways via which foraging conditions and predictive cues such as photoperiod enforce seasonality, (ii) considers the kinds of seasonal challenges mammals actually face in natural habitats, and (iii) uses the information thus generated to suggest how seasonal reproduction might be influenced by global climate change. Food availability and ambient temperature determine energy balance, and variation in energy balance is the ultimate cause of seasonal breeding in all mammals and the proximate cause in many. Photoperiodic cueing is common among long-lived mammals from the highest latitudes down to the mid-tropics. It is much less common in shorter lived mammals at all latitudes. An unknown predictive cue triggers reproduction in some desert and dry grassland species when it rains. The available information suggests that as our climate changes the small rodents of the world may adapt rather easily but the longer lived mammals whose reproduction is regulated by photoperiod may not do so well. A major gap in our knowledge concerns the tropics; that is where most species live and where we have the least understanding of how reproduction is regulated by environmental factors.     

Carbon emissions performance of commercial logging in East Kalimantan,Indonesia

Adoption of reduced‐impact logging (RIL) methods could reduce CO₂ emissions by 30–50% across at least 20% of remaining tropical forests. We developed two cost effective and robust indices for comparing the climate benefits (reduced CO₂ emissions) due to RIL. The indices correct for variability in the volume of commercial timber among concessions. We determined that a correction for variability in terrain slope was not needed. We found that concessions certified by the Forest Stewardship Council (FSC, N = 3), when compared with noncertified concessions (N = 6), did not have lower overall CO₂ emissions from logging activity (felling, skidding, and hauling). On the other hand, FSC certified concessions did have lower emissions from one type of logging impact (skidding), and we found evidence of a range of improved practices using other field metrics. One explanation of these results may be that FSC criteria and indicators, and associated RIL practices, were not designed to achieve overall emissions reductions. Also, commonly used field metrics are not reliable proxies for overall logging emissions performance. Furthermore, the simple distinction between certified and noncertified concessions does not fully represent the complex history of investments in improved logging practices. To clarify the relationship between RIL and emissions reductions, we propose the more explicit term ‘RIL‐C’ to refer to the subset of RIL practices that can be defined by quantified thresholds and that result in measurable emissions reductions. If tropical forest certification is to be linked with CO₂ emissions reductions, certification standards need to explicitly require RIL‐C practices.     

Lability of fat stores in peripubertal wild house mice

Summary Traditionally, the adaptive value of mammalian white fat stores is considered in relation to longterm needs such as providing protection against the vagaries of winter or signalling the reproductive system when energy reserves are sufficient to risk pregnancy. As shown here, the fat stores of young house mice could not serve such needs. Despite prolonged acclimation and excess nesting material, food deprivation at 10°C significantly lowered the fat stores of peripubertal female house mice in only 12 h, and would exhaust them in 30 h. Even close to thermoneutrality (24°C) the calculated time to exhaustion was only 70 h. The fat stores of a young house mouse are obviously too meager to offer any meaningful protection over a winter of several months duration, or even over a 5–6-week cycle of pregnancy and lactation. Furthermore, in a wild habitat where food availability and ambient temperature can vary rapidly and greatly, such fat stores would be too labile to effectively coordinate puberty with somatic development.     

Genetic Characteristics of Restored Elk Populations in Kentucky

Translocations are a common management practice to restore or augment populations. Understanding the genetic consequences of translocation efforts is important for the long-term health of restored populations. The restoration of elk (Cervus canadensis) to Kentucky, USA, included source stocks from 6 western states, which were released at 8 sites in southeastern Kentucky during 1997–2002. We assessed genetic diversity in restored herds and compared genetic similarity to source stocks based on 15 microsatellite DNA loci. Genetic variation in the restored populations was comparable to source stocks ( allelic richness = 3.52 and 3.50; expected heterozygosity = 0.665 and 0.661 for restored and source, respectively). Genetic differentiation among all source and restored populations ranged from 0.000 to 0.065 for pairwise F_ST and 0.034 to 0.161 for pairwise Nei's D_A. Pairwise genetic differentiation and Bayesian clustering revealed that stocks from Utah and North Dakota, USA, contributed most to restored populations. Other western stocks appeared less successful and were not detected with our data, though our sampling was not exhaustive. We also inferred natural movements of elk among release sites by the presence of multiple genetic stocks. The success of the elk restoration effort in Kentucky may be due, in part, to the large number of elk (n = 1,548), repeated releases, and use of diverse source stocks. Future restoration efforts for elk in the eastern United States should consider the use of multiple stock sources and a large number of individuals. In addition, preservation of genetic samples of founder stock will enable detailed monitoring in the future. © 2020 The Authors. The Journal of Wildlife Management published by Wiley Periodicals, Inc. on behalf of The Wildlife Society.     

Miniature Swine as a Clinically Relevant Model of Graft-Versus-Host Disease

Miniature swine provide a preclinical model of hematopoietic cell transplantation (HCT) for studies of graft-versus-host disease. HCT between MHC-matched or ‑mismatched pigs can be performed to mimic clinical scenarios with outcomes that closely resemble those observed in human HCT recipients. With myeloablative conditioning, HCT across MHC barriers is typically fatal, with pigs developing severe (grade III or IV) GVHD involving the gastrointestinal tract, liver, and skin. Unlike rodent models, miniature swine provide an opportunity to perform extended longitudinal studies on individual animals, because multiple tissue biopsies can be harvested without the need for euthanasia. In addition, we have developed a swine GVHD scoring system that parallels that used in the human clinical setting. Given the similarities of GVHD in pigs and humans, we hope that the use of this scoring system facilitates clinical and scientific discourse between the laboratory and the clinic. We anticipate that results of swine studies will support the development of new strategies to improve the identification and treatment of GVHD in clinical HCT scenarios.Abbreviations: BMT, bone marrow transplantation; GVHD, graft-versus-host disease; GVL, graft-versus-leukemia; HCT, hematopoietic cell transplantation; TBI, total-body irradiation     

Prdx1 inhibits tumorigenesis via regulating PTEN/AKT activity

It is widely accepted that reactive oxygen species (ROS) promote tumorigenesis. However, the exact mechanisms are still unclear. As mice lacking the peroxidase peroxiredoxin1 (Prdx1) produce more cellular ROS and die prematurely of cancer, they offer an ideal model system to study ROS‐induced tumorigenesis. Prdx1 ablation increased the susceptibility to Ras‐induced breast cancer. We, therefore, investigated the role of Prdx1 in regulating oncogenic Ras effector pathways. We found Akt hyperactive in fibroblasts and mammary epithelial cells lacking Prdx1. Investigating the nature of such elevated Akt activation established a novel role for Prdx1 as a safeguard for the lipid phosphatase activity of PTEN, which is essential for its tumour suppressive function. We found binding of the peroxidase Prdx1 to PTEN essential for protecting PTEN from oxidation‐induced inactivation. Along those lines, Prdx1 tumour suppression of Ras‐ or ErbB‐2‐induced transformation was mediated mainly via PTEN.