It is not always about body size: evidence of Rensch's rule in a male weapon

In many species, sexual dimorphism increases with body size when males are the larger sex but decreases when females are the larger sex, a macro-evolutionary pattern known as Rensch''s rule (RR). Although empirical studies usually focus exclusively on body size, Rensch''s original proposal included sexual differences in other traits, such as ornaments and weapons. Here, we used a clade of harvestmen to investigate whether two traits follow RR: body size and length of the fourth pair of legs (legs IV), which are used as weapons in male–male fights. We found that males were slightly smaller than females and body size did not follow RR, whereas legs IV were much longer in males and followed RR. We propose that sexual selection might be stronger on legs IV length than on body size in males, and we discuss the potential role of condition dependence in the emergence of RR.     

Prey selection by nesting House Martins Delichon urbica Linné, 1758 (Aves: Hirundinidae) in Algiers suburbs (Algeria)

The diet of the House Martin Delichon urbica was analyzed in a suburban area in Pins maritimes, northeast of Algiers (Algeria). The diet was determined by analyzing 120 faecal samples collected from a breeding colony between April and September 2007. Insects were the most numerous prey types (99.86%). Hymenopterans were the dominant preys (56.99%), followed by Coleopterans (20.14%), Homopterans (14.22%), Heteropterans (5.45%), and Dipterans (3.10%). Division of the prey items into families demonstrated that the highest relative frequency was large Hymenopterans in the family Formicidae (54.0%). The dominant species in the diet was Tetramorium biskrensis, which comprised 32.6% of the diet. It was followed by Camponotus barbaricus (6.9%) and Monomorium salomonis (5.6%). Comparison between diet and availability of preys using the Savage index showed that T. biskrensis, Crematogaster scutelaris, Pheidole pallidula, Diptera sp. unident. and Aphidae sp. unident. were positively selected by D. urbica.     

Trans‐species synthetic gene design allows resistance pyramiding and broad‐spectrum engineering of virus resistance in plants

To infect plants, viruses rely heavily on their host's machinery. Plant genetic resistances based on host factor modifications can be found among existing natural variability and are widely used for some but not all crops. While biotechnology can supply for the lack of natural resistance alleles, new strategies need to be developed to increase resistance spectra and durability without impairing plant development. Here, we assess how the targeted allele modification of the Arabidopsis thaliana translation initiation factor eIF4E1 can lead to broad and efficient resistance to the major group of potyviruses. A synthetic Arabidopsis thaliana eIF4E1 allele was designed by introducing multiple amino acid changes associated with resistance to potyvirus in naturally occurring Pisum sativum alleles. This new allele encodes a functional protein while maintaining plant resistance to a potyvirus isolate that usually hijacks eIF4E1. Due to its biological functionality, this synthetic allele allows, at no developmental cost, the pyramiding of resistances to potyviruses that selectively use the two major translation initiation factors, eIF4E1 or its isoform eIFiso4E. Moreover, this combination extends the resistance spectrum to potyvirus isolates for which no efficient resistance has so far been found, including resistance‐breaking isolates and an unrelated virus belonging to the Luteoviridae family. This study is a proof‐of‐concept for the efficiency of gene engineering combined with knowledge of natural variation to generate trans‐species virus resistance at no developmental cost to the plant. This has implications for breeding of crops with broad‐spectrum and high durability resistance using recent genome editing techniques.     

Biomarker potential of C-peptide for screening of insulin resistance in diabetic and non-diabetic individuals

Insulin resistance is a hallmark feature of type-2 diabetes mellitus (T2DM). We determined the homeostatic model assessment insulin resistance (HOMA-IR) and evaluated its association with C-peptide, insulin, fasting blood glucose (FBG) and glycated hemoglobin (HbA1c) in T2DM patients and non-diabetic subjects. This study comprised a total of 47 T2DM patients and 38 non-diabetic controls. Venous blood samples from all the subjects were collected and sera were analyzed for FBG, HbA1c, insulin and C-peptide using an autoanalyzer. HOMA-IR was calculated using the following equation: HOMA-IR?=?fasting insulin (µU/ml)?×?fasting glucose (mmol/L)/22.5. There was a significant increase in the levels of FBG and HbA1c in diabetic patients. Although the levels of C-peptide and insulin did not differ significantly between the two groups, a significant increase in HOMA-IR was observed in T2DM patients. Both insulin and C-peptide were significantly correlated with HOMA-IR. In conclusion, C-peptide may serve as a simple and convenient predictor of HOMA-IR.     

Direct molecular analysis of the fragile X syndrome in a sample of Egyptian and German patients using non-radioactive PCR and Southern blot followed by chemiluminescent detection

Molecular genetic analysis of individuals from 6 Egyptian and 33 German families with fragile X syndrome and 240 further patients with mental retardation was performed applying a completely non-radioactive system. The aim of our study was the development of a non-radioactive detection method and its implementation in molecular diagnosis of the fragile X syndrome. Furthermore, we wanted to assess differences in the mutation sizes between Egyptian and German patients and between Egyptian and German carriers of a premutation. Using non-radioactive polymerase chain reaction (PCR), agarose gel electrophoresis and blotting of the PCR products, followed by hybridisation with a digoxigenin-labelled oligonucleotide probe (CGG)₅ and chemiluminescent detection, we identified the fragile X full mutation (amplification of a CGG repeat in the FMR-1 gene ranging from several hundred to several thousand repeat units) in all patients. We observed no differences in the length of the CGG repeat between the Egyptian and German patients and carriers, respectively. However, in one prenatal diagnosis, we detected only one normal sized allele in a female fetus using the PCR-agarose assay, whereas Southern blot analysis with the digoxigenin labelled probe StB 12.3 revealed presence of a full mutation. Our newly established nonradioactive genomic blotting method is based on the conventional radioactive Southern blot analysis. Labelling of the probe StB 12.3 with digoxigenin via PCR allowed the detection of normal, premutated and fully mutated alleles. For exact sizing of small premutated or large normal alleles, we separated digoxigenin labelled PCR products through denaturing poly-acrylamide gelelectrophoresis (PAGE) and transfered them to a nylon membrane using a gel dryer. The blotted PCR-fragments can easily be detected with alkaline phosphate-labelled anti-digoxigenin antibody. The number of trinucleotide repeat units can be determined by scoring the detected bands against a digoxigenated M13 sequencing ladder. Our newly developed digoxigenin/chemiluminescence approach using PCR and Southern blot analysis provides reliable results for routine detection of full fragile X mutations and premutations.     

The Primordial Growth Disorder 3-M Syndrome Connects Ubiquitination to the Cytoskeletal Adaptor OBSL1

3-M syndrome is an autosomal-recessive primordial growth disorder characterized by significant intrauterine and postnatal growth restriction. Mutations in the CUL7 gene are known to cause 3-M syndrome. In 3-M syndrome patients that do not carry CUL7 mutations, we performed high-density genome-wide SNP mapping to identify a second locus at 2q35-q36.1. Further haplotype analysis revealed a 1.29 Mb interval in which the underlying gene is located and we subsequently discovered seven distinct null mutations from 10 families within the gene OBSL1. OBSL1 is a putative cytoskeletal adaptor protein that localizes to the nuclear envelope. We were also able to demonstrate that loss of OBSL1 leads to downregulation of CUL7, implying a role for OBSL1 in the maintenance of CUL7 protein levels and suggesting that both proteins are involved within the same molecular pathway.     

Dog Obesity: Can Dog Caregivers' (Owners') Feeding and Exercise Intentions and Behaviors Be Predicted From Attitudes?

Dog obesity is a common nutritional disorder affecting up to 40% of the companion animal (pet) dog population in Australia and other developed nations. A clear understanding of factors determining relevant caregiver (owner) behaviors underpins effective treatment for this disorder. The theory of planned behavior can be used to understand factors contributing to human behavior. This article describes research informed by this theory. The research examined relationships between owners' behavioral beliefs and barriers, normative beliefs and perceptions of control, owners' feeding and exercise behaviors toward their dogs, and the body condition scores (BCSs) of dogs. The study recruited a sample of 182 dog and owner dyads. The researcher independently assessed BCSs. Owners completed a questionnaire measuring relevant feeding and exercise beliefs and behaviors. This revealed significant correlations between many psychological variables and BCSs and between psychological variables and specific owner behaviors: for example, the relationship of low levels of intentions to feed appropriately to ambivalent beliefs toward feeding appropriately and low perceived control. Careful consideration of the specific variables identified will permit the development of more effective interventions.     

Proteomic profiling of the hypothalamus in two mouse models of narcolepsy

Narcolepsy is a disabling neurological disorder of sleepiness linked to the loss of neurons producing orexin neuropeptides in the hypothalamus. Two well‐characterized phenotypic mouse models of narcolepsy, loss‐of‐function (orexin‐knockout), and progressive loss of orexin (orexin/ataxin‐3) exist. The open question is whether the proteomics signatures of the hypothalamus would be different between the two models. To address this gap, we utilized a label‐free proteomics approach and conducted a hypothalamic proteome analysis by comparing each disease model to that of wild type. Following data processing and statistical analysis, 14 484 peptides mapping to 2282 nonredundant proteins were identified, of which 39 proteins showed significant differences in protein expression across groups. Altered proteins in both models showed commonalties in pathways for mitochondrial dysfunction and neuronal degeneration, as well as altered proteins related to inflammatory demyelination, insulin resistance, metabolic responses, and the dopaminergic and monoaminergic systems. Model‐specific alterations in insulin degraded enzyme (IDE) and synaptosomal‐associated protein‐25 were unique to orexin‐KO and orexin/ataxin‐3, respectively. For both models, proteomics not only identified clinically suspected consequences of orexin loss on energy homeostasis and neurotransmitter systems, but also identified commonalities in inflammation and degeneration despite the entirely different genetic basis of the two mouse models.