Comparative growth and static allometry in the genus Chlorocebus

Characterizing variation in growth across populations is critical to understanding multiple aspects of development in primates, including within-taxon developmental plasticity and the evolution of life history patterns. Growth in wild primates has often been reported and directly compared across larger taxonomic groups and within social groups, but comparisons are rarely investigated across widely dispersed populations of a single taxon. With the Vervet Phenome-Genome Project and the International Vervet Research Consortium, we trapped 936 vervet monkeys of all ages representing three populations (Kenyan pygerythrus, South African pygerythrus, and sabaeus from St. Kitts & Nevis). We gathered 10 different body measurements from each including mass, body breadth and length, segmental limb lengths, and chest circumference. To gain a better understanding of how ontogenetic patterns vary in these populations, we calculated bivariate allometry coefficients, derived using PCA on log-transformed and z-standardized trait values, and compared them to isometric vector coefficients. Within all population samples, around weaning age most traits showed a negative allometric relationship to body length. As each population ages, however, distinct patterns emerge, showing population differences in onset and intensity of growth among traits. In concordance with other analyses on growth in these populations, our results suggest that there exist relative differences in patterns of growth between Chlorocebus populations, further suggesting selection for unique developmental pathways in each

Inhibition of erythrocyte δ- aminolevulinic acid dehydratase (ALAD) activity in fish from waters affects by lead smelters

We assessed the effects on fish of lead (Pb) released to streams by smelters located in Trail, BC (Canada), E. Helena, MT, Herculaneum, MO, and Glover, MO. Fish were collected by electrofishing from sites located downstream of smelters and from reference sites. Blood from each fish was analyzed for δ-aminolevulinic acid dehydratase (ALAD) activity and hemoglobin (Hb), and samples of blood, liver, or carcass were analyzed for Pb, zinc (Zn), or both. Fish collected downstream of all four smelters sites had elevated Pb concentrations, decreased ALAD activity, or both relative to their respective reference sites. At E. Helena, fish from the downstream site also had lower Hb concentrations than fish from upstream. Differences among taxa were also apparent. Consistent with previous studies, ALAD activity in catostomids (Pisces: Catostomidae-northern hog sucker, Hypentelium nigricans; river carpsucker, Carpiodes carpio; largescale sucker, Catostomus macrocheilus; and mountain sucker, C. platyrhynchus) seemed more sensitive to Pb-induced ALAD inhibition than the salmonids (Pisces: Salmonidae-rainbow trout, Oncorhynchus mykiss; brook trout, Salvelinus fontinalis) or common carp (Cyprinus carpio). Some of these differences may have resulted from differential accumulation of Zn, which was not measured at all sites. We detected no ALAD activity in channel catfish (Ictalurus punctatus) from either site on the Mississippi River at Herculaneum, MO. Our findings confirmed that Pb is released to aquatic ecosystems by smelters and accumulated by fish, and we documented potentially adverse effects of Pb in fish. We recommend that Zn be measured along with Pb when ALAD activity is used as a biomarker and the collection of at least 10 fish of a species at each site to facilitate statistical analysis

Inhibition of erythrocyte δ- aminolevulinic acid dehydratase (ALAD) activity in fish from waters affects by lead smelters

We assessed the effects on fish of lead (Pb) released to streams by smelters located in Trail, BC (Canada), E. Helena, MT, Herculaneum, MO, and Glover, MO. Fish were collected by electrofishing from sites located downstream of smelters and from reference sites. Blood from each fish was analyzed for δ-aminolevulinic acid dehydratase (ALAD) activity and hemoglobin (Hb), and samples of blood, liver, or carcass were analyzed for Pb, zinc (Zn), or both. Fish collected downstream of all four smelters sites had elevated Pb concentrations, decreased ALAD activity, or both relative to their respective reference sites. At E. Helena, fish from the downstream site also had lower Hb concentrations than fish from upstream. Differences among taxa were also apparent. Consistent with previous studies, ALAD activity in catostomids (Pisces: Catostomidae-northern hog sucker, Hypentelium nigricans; river carpsucker, Carpiodes carpio; largescale sucker, Catostomus macrocheilus; and mountain sucker, C. platyrhynchus) seemed more sensitive to Pb-induced ALAD inhibition than the salmonids (Pisces: Salmonidae-rainbow trout, Oncorhynchus mykiss; brook trout, Salvelinus fontinalis) or common carp (Cyprinus carpio). Some of these differences may have resulted from differential accumulation of Zn, which was not measured at all sites. We detected no ALAD activity in channel catfish (Ictalurus punctatus) from either site on the Mississippi River at Herculaneum, MO. Our findings confirmed that Pb is released to aquatic ecosystems by smelters and accumulated by fish, and we documented potentially adverse effects of Pb in fish. We recommend that Zn be measured along with Pb when ALAD activity is used as a biomarker and the collection of at least 10 fish of a species at each site to facilitate statistical analysis

Distinct Patterns of Default Mode and Executive Control Network Circuitry Contribute to Present and Future Executive Function in Older Adults

Executive function (EF) performance in older adults has been linked with functional and structural profiles within the executive control network (ECN) and default mode network (DMN), white matter hyperintensities (WMH) burden and levels of Alzheimer\u27s disease (AD) pathology. Here, we simultaneously explored the unique contributions of these factors to baseline and longitudinal EF performance in older adults. Thirty-two cognitively normal (CN) older adults underwent neuropsychological testing at baseline and annually for three years. Neuroimaging and AD pathology measures were collected at baseline. Separate linear regression models were used to determine which of these variables predicted composite EF scores at baseline and/or average annual change in composite ΔEF scores over the three-year follow-up period. Results demonstrated that low DMN deactivation, high ECN activation and WMH burden were the main predictors of EF scores at baseline. In contrast, poor DMN and ECN WM microstructure and higher AD pathology predicted greater annual decline in EF scores. Subsequent mediation analysis demonstrated that DMN WM microstructure uniquely mediated the relationship between AD pathology and ΔEF. These results suggest that functional activation patterns within the DMN and ECN and WMHs contribute to baseline EF while structural connectivity within these networks impact longitudinal EF performance in older adults

The static allometry of sexual and non-sexual traits in vervet monkeys

Sexual traits vary tremendously in static allometry. This variation may be explained in part by body size-related differences in the strength of selection. We tested this hypothesis in two populations of vervet monkeys, using estimates of the level of condition dependence for different morphological traits as a proxy for body size-related variation in the strength of selection. In support of the hypothesis, we found that the steepness of allometric slopes increased with the level of condition dependence. One trait of particular interest, the penis, had shallow allometric slopes and low levels of condition dependence, in agreement with one of the most consistent patterns yet detected in the study of allometry, namely that of genitalia exhibiting shallow allometries.This research was supported by NIH grant R01RR0163009

The integration of quantitative genetics, paleontology, and neontology reveals genetic underpinnings of primate dental evolution

Significance Experimental research on mice has yielded tremendous biological insight. However, the ∼140 million y of evolution that separate mice from humans pose a hurdle to direct application of this knowledge to humans. We report here that considerable progress for identifying genetically patterned skeletal phenotypes beyond the mouse model is possible through transdisciplinary approaches that include the anatomical sciences. Indeed, anatomy and paleontology offer unique opportunities through which to develop and test hypotheses about the underlying genetic mechanisms of the skeleton for taxa that are not well suited to experimental manipulation, such as ourselves. Abstract Developmental genetics research on mice provides a relatively sound understanding of the genes necessary and sufficient to make mammalian teeth. However, mouse dentitions are highly derived compared with human dentitions, complicating the application of these insights to human biology. We used quantitative genetic analyses of data from living nonhuman primates and extensive osteological and paleontological collections to refine our assessment of dental phenotypes so that they better represent how the underlying genetic mechanisms actually influence anatomical variation. We identify ratios that better characterize the output of two dental genetic patterning mechanisms for primate dentitions. These two newly defined phenotypes are heritable with no measurable pleiotropic effects. When we consider how these two phenotypes vary across neontological and paleontological datasets, we find that the major Middle Miocene taxonomic shift in primate diversity is characterized by a shift in these two genetic outputs. Our results build on the mouse model by combining quantitative genetics and paleontology, and thereby elucidate how genetic mechanisms likely underlie major events in primate evolution

Folding-competent and folding-defective forms of Ricin A chain have different fates following retrotranslocation from the endoplasmic reticulum

We report that a toxic polypeptide retaining the potential to refold upon dislocation from the endoplasmic reticulum (ER) to the cytosol (ricin A chain; RTA) and a misfolded version that cannot (termed RTAΔ), follow ER-associated degradation (ERAD) pathways in Saccharomyces cerevisiae that substantially diverge in the cytosol. Both polypeptides are dislocated in a step mediated by the transmembrane Hrd1p ubiquitin ligase complex and subsequently degraded. Canonical polyubiquitylation is not a prerequisite for this interaction because a catalytically inactive Hrd1p E3 ubiquitin ligase retains the ability to retrotranslocate RTA, and variants lacking one or both endogenous lysyl residues also require the Hrd1p complex. In the case of native RTA, we established that dislocation also depends on other components of the classical ERAD-L pathway as well as an ongoing ER–Golgi transport. However, the dislocation pathways deviate strikingly upon entry into the cytosol. Here, the CDC48 complex is required only for RTAΔ, although the involvement of individual ATPases (Rpt proteins) in the 19S regulatory particle (RP) of the proteasome, and the 20S catalytic chamber itself, is very different for the two RTA variants. We conclude that cytosolic ERAD components, particularly the proteasome RP, can discriminate between structural features of the same substrate