Quantitative Genetics, Pleiotropy, and Morphological Integration in the Dentition of Papio hamadryas

Variation in the mammalian dentition is highly informative of adaptations and evolutionary relationships, and consequently has been the focus of considerable research. Much of the current research exploring the genetic underpinnings of dental variation can trace its roots to Olson and Miller's 1958 book Morphological Integration. These authors explored patterns of correlation in the post-canine dentitions of the owl monkey and Hyopsodus, an extinct condylarth from the Eocene. Their results were difficult to interpret, as was even noted by the authors, due to a lack of genetic information through which to view the patterns of correlation. Following in the spirit of Olson and Miller's research, we present a quantitative genetic analysis of dental variation in a pedigreed population of baboons. We identify patterns of genetic correlations that provide insight to the genetic architecture of the baboon dentition. This genetic architecture indicates the presence of at least three modules: an incisor module that is genetically independent of the post-canine dentition, and a premolar module that demonstrates incomplete pleiotropy with the molar module. We then compare this matrix of genetic correlations to matrices of phenotypic correlations between the same measurements made on museum specimens of another baboon subspecies and the Southeast Asian colobine Presbytis. We observe moderate significant correlations between the matrices from these three primate taxa. From these observations we infer similarity in modularity and hypothesize a common pattern of genetic integration across the dental arcade in the Cercopithecoidea

Please Don’t Leave Me—Separation Anxiety and Related Traits in Borderline Personality Disorder

Purpose of Review: In light of the apparent symptomatic resemblance of separation anxiety disorder (SAD) symptoms on the one hand and abandonment fears, anxiousness, and separation insecurity central to borderline personality disorder (BPD) on the other hand, a comprehensive overview of separation anxiety and related traits in BPD is provided. Recent Findings: Epidemiological, environmental, psychological, and neurobiological data connecting BPD to separation events, feelings of loneliness, insecure attachment styles, dimensional separation anxiety as well as SAD per se suggest a partly shared etiological pathway model underlying BPD and SAD. Differential diagnostic aspects and implications for treatment are discussed, highlighting separation anxiety as a promising transdiagnostic target for specific psychotherapeutic and pharmacological treatment approaches in BPD. Summary: This innovative angle on cross-disorder symptomatology might carry potential for novel preventive and therapeutic avenues in clinical practice by guiding the development of interventions specifically targeting separation anxiety and attachment-related issues in BPD

Myocardial Mitochondrial and Contractile Function Are Preserved in Mice Lacking Adiponectin

<div><p>Adiponectin deficiency leads to increased myocardial infarct size following ischemia reperfusion and to exaggerated cardiac hypertrophy following pressure overload, entities that are causally linked to mitochondrial dysfunction. In skeletal muscle, lack of adiponectin results in impaired mitochondrial function. Thus, it was our objective to investigate whether adiponectin deficiency impairs mitochondrial energetics in the heart. At 8 weeks of age, heart weight-to-body weight ratios were not different between adiponectin knockout (ADQ^-/-) mice and wildtypes (WT). In isolated working hearts, cardiac output, aortic developed pressure and cardiac power were preserved in ADQ^-/- mice. Rates of fatty acid oxidation, glucose oxidation and glycolysis were unchanged between groups. While myocardial oxygen consumption was slightly reduced (-24%) in ADQ^-/- mice in isolated working hearts, rates of maximal ADP-stimulated mitochondrial oxygen consumption and ATP synthesis in saponin-permeabilized cardiac fibers were preserved in ADQ^-/- mice with glutamate, pyruvate or palmitoyl-carnitine as a substrate. In addition, enzymatic activity of respiratory complexes I and II was unchanged between groups. Phosphorylation of AMP-activated protein kinase and SIRT1 activity were not decreased, expression and acetylation of PGC-1α were unchanged, and mitochondrial content of OXPHOS subunits was not decreased in ADQ^-/- mice. Finally, increasing energy demands due to prolonged subcutaneous infusion of isoproterenol did not differentially affect cardiac contractility or mitochondrial function in ADQ^-/- mice compared to WT. Thus, mitochondrial and contractile function are preserved in hearts of mice lacking adiponectin, suggesting that adiponectin may be expendable in the regulation of mitochondrial energetics and contractile function in the heart under non-pathological conditions.</p></div

Preserved mitochondrial function in ADQ^-/- hearts following isoproterenol treatment.

<p>Mitochondrial O₂ consumption rates (A), ATP synthesis rates (B), and ATP/O ratios (C) in saponin-permeabilized cardiac fibers of ADQ^-/- and WT mice using glutamate as substrate; n = 4. 2-way ANOVA: § effect of isoproterenol.</p

Preserved mitochondrial OXPHOS complex activities in ADQ^-/- hearts.

<p>Enzymatic activity of complex I subunit NDUFB8 (A), complex II subunit 30kDa (B), and complex IV subunit II (C) in isolated mitochondria of ADQ^-/- and WT hearts; n = 5–6. * p<0.05 vs. WT.</p

Preserved mitochondrial function in ADQ^-/- hearts.

<p>Mitochondrial O₂ consumption rates, ATP synthesis rates, and ATP/O ratios in saponin-permeabilized cardiac fibers of ADQ^-/- and WT mice, using palmitoyl-carnitine (A-C), glutamate (D-F), or pyruvate (G-I) as substrate; n = 6.</p

Preserved OXPHOS protein levels and mitochondrial biogenic signaling in ADQ^-/- hearts.

<p>AMPK phosphorylation (A), SIRT1 activity (B), lysine acetylation (Lys-Ac) of PGC-1α (C), mRNA expression of OXPHOS subunits (D), mRNA expression of mitochondrial biogenesis signaling molecules (E), mRNA expression of fatty acid oxidation genes and PPARα (F), and mitochondrial protein levels of OXPHOS complexes I (NDUFB8 subunit; G), II (Fp subunit; H), and IV (subunit IV; I) in hearts of ADQ^-/- and WT mice at 8 weeks of age; n = 4–5. Myocardial mRNA expression is expressed relative to WT expression which was set to 1 (indicated by the dotted line). * p<0.05 vs. WT.</p

Preserved contractile function in ADQ^-/- hearts.

<p>Cardiac power (A), aortic developed pressure (B), cardiac output (C), palmitate oxidation (D), glucose oxidation (E), glycolysis (F), MVO₂ (G), and cardiac efficiency (H) in isolated working hearts of ADQ^-/- and WT mice at 8 weeks of age; n = 4–6 for substrate oxidation, n = 10 for contractile parameters. (I) Myocardial triacylglycerol levels in ADQ^-/- and WT mice at 8 weeks of age; n = 4–5. * p<0.05 vs. WT.</p