Whales in warming water: Assessing breeding habitat diversity and adaptability in Oceania's changing climate

In the context of a changing climate, understanding the environmental drivers of marine megafauna distribution is important for conservation success. The extent of humpback whale breeding habitats and the impact of temperature variation on their availability are both unknown. We used 19 years of dedicated survey data from seven countries and territories of Oceania (1,376 survey days), to investigate humpback whale breeding habitat diversity and adaptability to climate change. At a fine scale (1 km resolution), seabed topography was identified as an important influence on humpback whale distribution. The shallowest waters close to shore or in lagoons were favored, although humpback whales also showed flexible habitat use patterns with respect to shallow offshore features such as seamounts. At a coarse scale (1° resolution), humpback whale breeding habitats in Oceania spanned a thermal range of 22.3–27.8°C in August, with interannual variation up to 2.0°C. Within this range, both fine and coarse scale analyses of humpback whale distribution suggested local responses to temperature. Notably, the most detailed dataset was available from New Caledonia (774 survey days, 1996–2017), where encounter rates showed a negative relationship to sea surface temperature, but were not related to the El Niño Southern Oscillation or the Antarctic Oscillation from previous summer, a proxy for feeding conditions that may impact breeding patterns. Many breeding sites that are currently occupied are predicted to become unsuitably warm for this species (>28°C) by the end of the 21st century. Based on modeled ecological relationships, there are suitable habitats for relocation in archipelagos and seamounts of southern Oceania. Although distribution shifts might be restrained by philopatry, the apparent plasticity of humpback whale habitat use patterns and the extent of suitable habitats support an adaptive capacity to ocean warming in Oceania breeding grounds.     

Divergent cellular phenotypes of human and mouse cells lacking the Werner syndrome RecQ helicase

Werner syndrome (WS) is a human autosomal recessive genetic instability and cancer predisposition syndrome with features of premature aging. Several genetically determined mouse models of WS have been generated, however, none develops features of premature aging or an elevated risk of neoplasia unless additional genetic perturbations are introduced. In order to determine whether differences in cellular phenotype could explain the discrepant phenotypes of Wrn^?/? mice and WRN-deficient humans, we compared the cellular phenotype of newly derived Wrn^?/? mouse primary fibroblasts with previous analyses of primary and transformed fibroblasts from WS patients and with newly derived, WRN-depleted human primary fibroblasts. These analyses confirmed previously reported cellular phenotypes of WRN-mutant and WRN-deficient human fibroblasts, and demonstrated that the human WRN-deficient cellular phenotype can be detected in cells grown in 5% or in 20% oxygen. In contrast, we did not identify prominent cellular phenotypes present in WRN-deficient human cells in Wrn^?/? mouse fibroblasts. Our results indicate that human and mouse fibroblasts have different functional requirements for WRN protein, and that the absence of a strong cellular phenotype may in part explain the failure of Wrn^?/? mice to develop an organismal phenotype resembling Werner syndrome.     

Genetic and developmental basis of cichlid trophic diversity

Cichlids have undergone extensive evolutionary modifications of their feeding apparatus, making them an ideal model to study the factors that underlie craniofacial diversity. Recent studies have provided critical insights into the molecular mechanisms that have contributed to the origin and maintenance of cichlid trophic diversity. We review this body of work, which shows that the cichlid jaw is regulated by a few genes of major additive effect, and is composed of modules that have evolved under strong divergent selection. Adaptive variation in cichlid jaw shape is evident early in development and is associated with allelic variation in and expression of bmp4. Modulating this growth factor in the experimentally tractable zebrafish model reproduces natural variation in cichlid jaw shape, supporting a role for bmp4 in craniofacial evolution. These data demonstrate the utility of the cichlid jaw as a model for studying the genetic and developmental basis of evolutionary changes in craniofacial morphology.     

Hybridization Promotes Evolvability in African Cichlids: Connections Between Transgressive Segregation and Phenotypic Integration

Hybridization is a potential source of novel variation through (1) transgressive segregation, and (2) changes in the patterns and strength of phenotypic integration. We investigated the capacity of hybridization to generate novel phenotypic variation in African cichlids by examining a large F2 population generated by hybridizing two Lake Malawi cichlid species with differently shaped heads. Our morphometric analysis focused on the lateral and ventral views of the head. While the lateral view exhibited marked transgressive segregation, the ventral view showed a limited ability for transgression, indicating a difference in the genetic architecture and selective history between alternate views of the head. Moreover, hybrids showed a marked reduction in integration, with a lower degree of integration observed in transgressive individuals. In all, these data offer novel insights into how hybridization can promote evolvability, and provide a possible explanation for how broad phenotypic diversity may be achieved in rapidly evolving groups.     

The potential role of swift foxes (Vulpes velox) and their fleas in plague outbreaks in prairie dogs

Swift foxes (Vulpes velox) have been proposed as potential carriers of fleas infected with the bacterium Yersinia pestis between areas of epizootics in black-tailed prairie dogs (Cynomys ludovicianus). We examined antibody prevalence rates of a population of swift foxes in Colorado, USA, and used polymerase chain reaction (PCR) assays to examine their flea biota for evidence of Y. pestis. Fifteen of 61 (24%) captured foxes were seropositive, and antibody prevalence was spatially correlated with epizootic plague activity in prairie dog colonies in the year of, and previous to, the study. Foxes commonly harbored the flea Pulex simulans, though none of the fleas was positive for Y. pestis.     

Evolution of a soft‐tissue foraging adaptation in African cichlids: Roles for novelty,convergence, and constraint

Understanding the origins of biodiversity demands consideration of both extrinsic (e.g., ecological opportunity) and intrinsic (e.g., developmental constraint) factors. Here, we use a combination of phylogenetic and genetic tools to address the origin of novelty in African cichlids. In particular, we focus on an extreme hypertrophied snout that is structurally integrated with the upper jaw. We show that this bizarre trait has evolved independently in at least two distinct and ecologically successful cichlid clades. We find that snout dimensions are decoupled both phenotypically and genetically, which has enabled it to evolve independently in multiple directions. Further, patterns of variation among species and within a genetic mapping pedigree suggest that relative to snout length, depth is under greater genetic and/or developmental constraint. Models of evolution suggest that snout shape is under selection for feeding behavior, with snout depth being important for algae scraping and snout length for sand sifting. Indeed, the deep snout of some algivores is achieved via an expansion of the intermaxillary ligament, which is important for jaw stability and may increase feeding performance. Overall, our data imply that the evolution of exaggerated snout depth required overcoming a genetic/developmental constraint, which led to expanded ecological opportunity via foraging adaptation.     

Localization of the ribosomal genes in Caenorhabditis elegans chromosomes by in situ hybridization using biotin-labeled probes

The site of the ribosomal gene cluster on embryonic metaphase chromosomes of Caenorhabditis elegans has been mapped by in situ hybridization using probe DNAs that have been nick-translated to incorporate biotin-labeled UTP. The hybridized probe DNA was detected by a double-layer fluorescent antibody technique. Since chromosomes from wild-type C. elegans embryos are indistinguishable, in situ hybridization was carried out with chromosomes from C. elegans strains carrying cytologically distinct translocation or duplication chromosomes in order to identify the right end of linkage group I as the site of the ribosomal genes. Chromosomes carrying a lethal mutation, let-209 I displayed smaller hybridization signals than wild-type, suggesting that these chromosomes carried a partial deficiency of the ribosomal gene cluster. A duplication of the ribosomal genes, eDp20(I;II) rescued let-209 homozygotes. Chromosomes carrying the alterations in the ribosomal genes were combined with mnT12(IV;X) to facilitate the mapping of genes in C. elegans by in situ hybridization. Linkage groups I and II are then labeled by the distinctive hybridization signals from the ribosomal probes, linkage groups IV and X are together distinguishable morphologically and linkage group V is labeled by hybridization to a 5S gene probe.