The evolution of color vision in nocturnal mammals

Nonfunctional visual genes are usually associated with species that inhabit poor light environments (aquatic/subterranean/nocturnal), and these genes are believed to have lost function through relaxed selection acting on the visual system. Indeed, the visual system is so adaptive that the reconstruction of intact ancestral opsin genes has been used to reject nocturnality in ancestral primates. To test these assertions, we examined the functionality of the short and medium- to long-wavelength opsin genes in a group of mammals that are supremely adapted to a nocturnal niche: the bats. We sequenced the visual cone opsin genes in 33 species of bat with diverse sensory ecologies and reconstructed their evolutionary history spanning 65 million years. We found that, whereas the long-wave opsin gene was conserved in all species, the short-wave opsin gene has undergone dramatic divergence among lineages. The occurrence of gene defects in the short-wave opsin gene leading to loss of function was found to directly coincide with the origin of high-duty-cycle echolocation and changes in roosting ecology in some lineages. Our findings indicate that both opsin genes have been under purifying selection in the majority bats despite a long history of nocturnality. However, when spectacular losses do occur, these result from an evolutionary sensory modality tradeoff, most likely driven by subtle shifts in ecological specialization rather than a nocturnal lifestyle. Our results suggest that UV color vision plays a considerably more important role in nocturnal mammalian sensory ecology than previously appreciated and highlight the caveat of inferring light environments from visual opsins and vice versa.     

Motion vision is independent of color in Drosophila

Whether motion vision uses color contrast is a controversial issue that has been investigated in several species, from insects to humans. We used Drosophila to answer this question, monitoring the optomotor response to moving color stimuli in WT and genetic variants. In the fly eye, a motion channel (outer photoreceptors R1-R6) and a color channel (inner photoreceptors R7 and R8) have been distinguished. With moving bars of alternating colors and high color contrast, a brightness ratio of the two colors can be found, at which the optomotor response is largely missing (point of equiluminance). Under these conditions, mutant flies lacking functional rhodopsin in R1-R6 cells do not respond at all. Furthermore, genetically eliminating the function of photoreceptors R7 and R8 neither alters the strength of the optomotor response nor shifts the point of equiluminance. We conclude that the color channel (R7/R8) does not contribute to motion detection as monitored by the optomotor response.     

The two-domain tree of life is linked to a new root for the Archaea

One of the most fundamental questions in evolutionary biology is the origin of the lineage leading to eukaryotes. Recent phylogenomic analyses have indicated an emergence of eukaryotes from within the radiation of modern Archaea and specifically from a group comprising Thaumarchaeota/“Aigarchaeota” (candidate phylum)/Crenarchaeota/Korarchaeota (TACK). Despite their major implications, these studies were all based on the reconstruction of universal trees and left the exact placement of eukaryotes with respect to the TACK lineage unclear. Here we have applied an original two-step approach that involves the separate analysis of markers shared between Archaea and eukaryotes and between Archaea and Bacteria. This strategy allowed us to use a larger number of markers and greater taxonomic coverage, obtain high-quality alignments, and alleviate tree reconstruction artifacts potentially introduced when analyzing the three domains simultaneously. Our results robustly indicate a sister relationship of eukaryotes with the TACK superphylum that is strongly associated with a distinct root of the Archaea that lies within the Euryarchaeota, challenging the traditional topology of the archaeal tree. Therefore, if we are to embrace an archaeal origin for eukaryotes, our view of the evolution of the third domain of life will have to be profoundly reconsidered, as will many areas of investigation aimed at inferring ancestral characteristics of early life and Earth.As was suggested by a few early phylogenetic analyses (1–3), over the past five years a number of universal trees of life rooted on the branch leading to Bacteria have supported an emergence of eukaryotes from within the radiation of modern Archaea (4–11), with a specific link to a group comprising Thaumarchaeota/“Aigarchaeota” (candidate phylum)/Crenarchaeota/Korarchaeota (the TACK superphylum) (5). This finding has very important consequences, because it clearly defines that an organism endowed with characteristics of a modern archaeon was the starting point for the process of eukaryogenesis (12, 13). Although these analyses used sophisticated approaches, they were all based on the reconstruction of universal trees of life and a restricted taxonomic sampling, in particular for the bacterial outgroup. Moreover, these studies have left the precise relationship of eukaryotes with the TACK lineages unclear (10) and showed intradomain phylogenies that were only partially resolved and often inconsistent between different analyses and with well-established relationships. In fact, analyzing the three domains at once reduces the number of markers and unambiguously aligned positions that can be used for phylogenetic reconstruction and may produce artifacts because of the very large interdomain distances (14). Furthermore, the inclusion of very fast-evolving lineages may distort the phylogeny within each domain and bias the inference of interdomain relationships. Such is the case, for example, of the recently proposed archaeal superphylum DPANN (Diapherotrites, Parvarchaeota, Aenigmarchaeota, Nanohaloarchaeota, and Nanoarchaeota) (15), which has shown conflicting placements in recent universal trees (9, 11), and may not even be monophyletic. Finally, the use of very restricted taxonomic sampling, notably for the outgroup, may also generate or mask potential tree reconstruction artifacts (16). All these considerations emphasize that we have not yet found a way out of the phylogenomic impasse caused by the use of universal trees to investigate the relationships among Archaea and eukaryotes (12).Here, we have applied an original two-step strategy that we proposed a few years ago which involves separately analyzing the markers shared between Archaea and eukaryotes and between Archaea and Bacteria (12). This strategy allowed us to use a larger taxonomic sampling, more markers and thus more positions, have higher-quality alignments, and detect potential tree reconstruction artifacts more easily. With respect to previous analyses, we obtained phylogenies that are fully resolved and consistent between datasets and with the systematics of each domain, demonstrating the relevance of our approach. Comparison of the results obtained from the Archaea/eukaryote (A/E) and the Archaea/Bacteria (A/B) datasets robustly indicates that eukaryotes are sister to the TACK superphylum but also that this topology is strongly linked to a root for the tree of the Archaea lying within the Euryarchaeota. This topology is in contrast to the traditional root between Euryarchaeota and the TACK superphylum (17, 18), which we demonstrate as likely being the product of an artifact resulting from the combination of noise introduced by fast-evolving positions and the use of an overly simplistic evolutionary model.     

Degenerate evolution of the hedgehog gene in a hemichordate lineage

The discovery of a set of highly conserved genes implicated in patterning during animal development represents one of the most striking findings from the field of evolutionary developmental biology. Existence of these “developmental toolkit” genes in diverse taxa, however, does not necessarily imply that they always perform the same functions. Here, we demonstrate functional evolution in a major toolkit gene. hedgehog (hh) encodes a protein that undergoes autocatalytic cleavage, releasing a signaling molecule involved in major developmental processes, notably neural patterning. We find that the hh gene of a colonial pterobranch hemichordate, Rhabdopleura compacta, is expressed in a dramatically different pattern to its ortholog in a harrimaniid enteropneust hemichordate, Saccoglossus kowalevskii. These represent two of the three major hemichordate lineages, the third being the indirect developing ptychoderid enteropneusts. We also show that the normally well-conserved amino acid sequence of the autoproteolytic cleavage site has a derived change in S. kowalevskii. Using ectopic expression in Drosophila, we find that this amino acid substitution reduces the efficiency of Hh autocatalytic cleavage and its signaling function. We conclude that the Hh sequence and expression in S. kowalevskii represent the derived state for deuterostomes, and we argue that functional evolution accompanied secondary reduction of the central nervous system in harrimaniids.     

The evolution of severe steatosis after bariatric surgery is related to insulin resistance

BACKGROUND & AIMS: In severely obese patients, factors implicated in the evolution of severe steatosis after bariatric surgery remain unresolved. Our aim was to determine whether insulin resistance (IR) influences the histologic effects induced by bariatric surgery. METHODS: We prospectively included 185 severely obese patients (body mass index >/=35 kg/m(2)) referred for bariatric surgery. The evolution of IR (IR index = 1/quantitative insulin sensitivity check index) and liver injury with consecutive biopsy was concomitantly assessed before and 1 year after surgery. RESULTS: At preoperative biopsy, 27% of severely obese patients disclosed severe steatosis (>/=60%). The alanine aminotransferase (P = .01) and IR indexes (P = .04) were independent predictive factors of severe steatosis at baseline. One year after surgery, surgical treatment induced a decrease in body mass index (9.5 kg/m(2); P < .0001), steatosis score (8.5%; P < .0001), and IR index (0.29; P < .0001). The preoperative IR index (P = .01) and preoperative steatosis (P = .006) were independent predictive factors in the persistence of severe steatosis after surgery. Moderate or severe steatosis was more frequently observed in patients who had conserved a higher IR index after surgery than in patients who had improved their IR index (44% vs 20.2%; P = .04). CONCLUSIONS: IR was independently associated with severe steatosis and predicted its persistence after surgery. The amelioration of IR after surgery is associated with a decrease in the amount of fat. Taken together, the results of this prospective study in severely obese patients demonstrate that severe steatosis and its evolution after surgery are intimately connected with IR.     

The development of antiphospholipid antibodies in haemophilia is linked to infection with hepatitis C

Summary In haemophilia the presence of antibodies to antiphospholipid has been linked with HIV infection, but other possibilities have not been fully explored and the specificity for various phospholipids not established. In order to investigate further the pathogenesis and clinical significance of these antibodies, we have determined IgG and IgM antibodies to a variety of phospholipids, including cardiolipin, in the serum of 52 haemophiliacs, and related our findings to the presence of antibodies to HIV and hepatitis C virus (HCV), as well as to clotting factor concentrate usage and blood markers of liver biochemistry. Our results demonstrate that the presence of infection with hepatitis C virus is strongly associated with raised serum levels of antiphospholipid antibody even in the absence of HIV infection. They suggest that earlier conclusions on the relationships of antiphospholipid to HIV infection in haemophilia should be revised and that chronic infection with the hepatitis C virus should be added to the list of infective cause for the development of angtiphospholipid antibody.     

Serum low-density lipoprotein cholesterol level is strong risk factor for acquired color vision impairment in young to middle-aged Japanese men: The Okubo Color Study Report 2

Objective

To investigate associations between blood low-density lipoprotein cholesterol (LDL-C) levels and the prevalence of acquired color vision impairment (ACVI) in middle-aged Japanese men.

Methods

Participants in this cross-sectional study underwent color vision testing, ophthalmic examination, a standardized interview and examination of venous blood samples. Ishihara plates, a Lanthony 15-hue desaturated panel, and Standard pseudoisochromatic Plates part 2 were used to examine color vision ability. The Farnsworth–Munsell 100-hue test was performed to define ACVI. Smoking status and alcohol intake were recorded during the interview. We performed logistic regression analysis adjusted for age, LDL-C level, systemic hypertension, diabetes, cataract, glaucoma, overweight, smoking status, and alcohol intake. Adjusted odds ratios for four LDL-C levels were calculated.

Results

A total of 1042 men were enrolled, 872 participants were eligible for the study, and 31 subjects were diagnosed with ACVI. As compared to the lowest LDL-C category level (<100 mg/dl), the crude OR of ACVI was 3.85 (95% confidence interval [CI], 1.24–11.00) for the 2nd highest category (130–159 mg/dl), and 4.84 (95% CI, 1.42–16.43) for the highest level (≥160 mg/dl). The multiple-adjusted ORs were 2.91 (95% CI, 0.87–9.70) for the 2nd highest category and 3.81 (95% CI, 1.03–14.05) for the highest level. Tests for trend were significant (P < 0.05) in both analyses.

Conclusions

These findings suggested that the prevalence of ACVI is higher among middle-aged Japanese men with elevated LDL-C levels. These changes might be related to deteriorated neurologic function associated with lipid metabolite abnormalities.     

The role of lateral erosion in the evolution of nondendritic drainage networks to dendricity and the persistence of dynamic networks

Dendritic, i.e., tree-like, river networks are ubiquitous features on Earth’s landscapes; however, how and why river networks organize themselves into this form are incompletely understood. A branching pattern has been argued to be an optimal state. Therefore, we should expect models of river evolution to drastically reorganize (suboptimal) purely nondendritic networks into (more optimal) dendritic networks. To date, current physically based models of river basin evolution are incapable of achieving this result without substantial allogenic forcing. Here, we present a model that does indeed accomplish massive drainage reorganization. The key feature in our model is basin-wide lateral incision of bedrock channels. The addition of this submodel allows for channels to laterally migrate, which generates river capture events and drainage migration. An important factor in the model that dictates the rate and frequency of drainage network reorganization is the ratio of two parameters, the lateral and vertical rock erodibility constants. In addition, our model is unique from others because its simulations approach a dynamic steady state. At a dynamic steady state, drainage networks persistently reorganize instead of approaching a stable configuration. Our model results suggest that lateral bedrock incision processes can drive major drainage reorganization and explain apparent long-lived transience in landscapes on Earth.

What should a drainage network look like? Fig. 1A shows a single channel, winding its way through the catchment so as to have access to water and sediment from unchannelized zones in the same manner as the dendritic (tree-like) network of Fig. 1B. It appears straightforward that the dendritic pattern is a model for nature, and the single channel is not. Dendritic drainage networks are called such because of their similarity to branching trees, and their patterns are “characterized by irregular branching in all directions” (1) with “tributaries joining at acute angles” (2). Drainage networks can also take on other forms such as parallel, pinnate, rectangular, and trellis in nature (2). However, drainage networks in their most basic form without topographic, lithologic, and tectonic constraints should tend toward a dendritic form (2). In addition, drainage networks that take a branching, tree-like form have been argued to be “optimal channel networks” that minimize total energy dissipation (3, 4). Therefore, we would expect that models simulating river network formation, named landscape evolution models (LEMs), that use the nondendritic pattern of Fig. 1A as an initial condition to massively reorganize and approach the dendritic steady state of Fig. 1B. To date, no numerical LEM has shown the ability to do this. Here, we present a LEM that can indeed accomplish such a reorganization. A corollary of this ability is the result that landscapes approach a dynamic, rather than static steady state.Open in a separate windowFig. 1.Schematic diagram of a nondendritic and a dendritic drainage network. This figure shows the Wolman Run Basin in Baltimore County, MD (A) drained by a single channel winding across the topography and (B) drained by a dendritic network of channels. Both networks have similar drainage densities (53, 54), but there is a stark difference between their stream ordering (53–56). This figure invites discussion as to how a drainage system might evolve from the configuration of A to that of B.There is indeed debate as to whether landscapes tend toward an equilibrium that is frozen or highly dynamic (5). Hack (6) hypothesized that erosional landscapes attain a steady state where “all elements of the topography are downwasting at the same rate.” This hypothesis has been tested in numerical models and small-scale experiments. Researchers found that numerical LEMs create static topographies (7, 8). In this state, erosion and uplift are in balance in all locations in the landscape, resulting in landscapes that are dissected by stable drainage networks in geometric equilibrium (9). The landscape has achieved geometric equilibrium in planform when a proxy for steady-state river elevation, named χ (10), has equal values across all drainage divides. In contrast, experimental landscapes (7, 11) develop drainage networks that persistently reorganize. Recent research on field landscapes suggests that drainage divides migrate until reaching geometric equilibrium (9), but other field-based research suggests that landscapes may never attain geometric equilibrium (12).The dynamism of the equilibrium state determines the persistence of initial conditions in experimental and model landscapes. It is important to understand initial condition effects (13) to better constrain uncertainty in LEM predictions. Kwang and Parker (7) demonstrate that numerical LEMs exhibit “extreme memory,” where small topographic perturbations in initial conditions are amplified and preserved during a landscape’s evolution (Fig. 2A). Extreme memory in the numerical models is closely related to the feasible optimality phenomenon found within the research on optimal channel networks (4). These researchers suggest that nature’s search for the most “stable” river network configuration is “myopic” and unable to find configurations that completely ignore their initial condition. In contrast to numerical models, experimental landscapes (7, 11) reach a highly dynamic state where all traces of initial surface conditions are erased by drainage network reorganization. It has been hypothesized that lateral erosion processes are responsible for drainage network reorganization in landscapes (7, 14); these processes are not included in most LEMs.Open in a separate windowFig. 2.A comparison of LEM-woLE (A) and LEM-wLE (B). Both models utilize the same initial condition, i.e., an initially flat topography with an embedded sinusoidal channel (1.27 m deep) without added topographic perturbations. Without perturbations, the landscape produces angular tributaries that are attached to the main sinusoidal channel (compare with SI Appendix, Fig. S7). Here, LEM-wLE quickly shreds the signal of the initial condition over time, removing the angular tributaries. By 10 RUs eroded the sinusoidal signal is mostly erased. After 100 RUs, the drainage network continues to reorganize itself (i.e., dynamic steady state). The landscape continues to reorganize as shown in Movies S1.Most widely used LEMs simulate incision into bedrock solely in the vertical direction. However, there is growing recognition that bedrock channels also shape the landscape by incising laterally (15, 16). Lateral migration into bedrock is important for the creation of strath terraces (17, 18) and the morphology of wide bedrock valleys (19–21). Recently, Langston and Tucker (22) developed a formulation for lateral bedrock erosion in LEMs. Here, we implement their submodel to explore the long-term behavior of LEMs that incorporate lateral erosion.The LEM submodel of Langston and Tucker (22) allows for channels to migrate laterally. By including this autogenic mechanism, we hypothesize that lateral bedrock erosion creates instabilities that 1) shred (23) the memory of initial conditions such as the unrealistic configurations of Fig. 1A and 2) produce landscapes that achieve a statistical steady state instead of a static one. By incorporating the lateral incision component (22) into a LEM, we aim to answer the following: 1) What controls the rate of decay of signals from initial conditions? 2) What are the frequency and magnitude of drainage reorganization in an equilibrium landscape? 3) What roles do model boundary conditions play in landscape reorganization?     

The balance of concurrent aggregation and deaggregation processes in platelets is linked to differential occupancy of ADP receptor subtypes

Deaggregation, the partial reversal of the initial aggregation of platelets is observed following low, but not higher, micromolar ADP concentrations. This study tested the hypothesis that deaggregation results from a balance between concurrent, opposing, aggregation and deaggregation processes which are ADP (adenosine 5'-diphosphate) receptor occupancy-dependent. Aggregation of human platelet-rich plasma (PRP) prepared in r-hirudin was assayed in a 96-well plate reader over 20 min by measurement of the optical density (OD) at 580 nm. Aggregation and the time to reach peak aggregation were directly proportional to ADP receptor occupancy. The magnitude and time course of the response to ADP were comparable to those previously reported with standard aggregometry. The rate constant of platelet deaggregation, as assessed by a fourcompartment kinetic model, was inversely proportional to agonist concentration. The ratio of the rate constants of aggregation and deaggregation was receptor occupancy-dependent and directly proportional to aggregation. Consequently, platelet aggregation was proportional, and deaggregation inversely proportional, to ADP receptor occupancy. We propose that the response of PRP to ADP and to 2-MeS-ADP (2-methylthioadenosinediphosphate), in vitro , consists of at least two active, concurrent processes, aggregation and deaggregation. Incremental occupancy of the P 2T ADP receptor subtype attenuates deaggregation and governs the balance between these two processes.     

The heart and heart conducting system in the kingdom of animals: A comparative approach to its evolution

The phylogeny of the heart and its conducting system is surveyed in the present study, as well as its parallels with ontogeny. A concise review of its evolution in the main taxonomic groups is presented. The aim is to inform physicians on evolutionary connections to the physiology of the human heart conducting system. Furthermore, some unanswered questions in terms of the developmental biology of the heart are offered. It is assumed that some supraventricular arrhythmias are based on remnants of embryonic structures of the pacemaking or conducting tissues; atrial flutter could re-entry through a survived embryonic sinoatrial ring. Some cases of atrial fibrillation could be initiated from remnant embryonic pacemaking cells settled in pulmonary veins.     

The D-allele of the ACE polymorphism is related to increased QT dispersion in 609 patients after myocardial infarction.

AIMS: Prolongation of QT dispersion can be observed in some patients with myocardial infarction and serves as a possible independent risk factor for sudden cardiac death. Angiotensin-converting enzyme (ACE) inhibition has been shown to reduce QT dispersion in myocardial infarction patients. We hypothesized that ACE gene I/D polymorphism, which is known to modulate ACE activity, may also affect QT dispersion after myocardial infarction. METHODS AND RESULTS: We studied 609 myocardial infarction patients (532 men, aged 56.1+/-0.3; mean 5.5 years after myocardial infarction) from a population-based myocardial infarction register by standardized questionnaire, anthropometry, ECG, echocardiography, and genotyping of ACE I/D polymorphism. In addition, 540 unaffected siblings (251 men, age 54.6+/-0.4 years) of these patients were studied by the same protocol. As compared with their healthy siblings, mean QT dispersion was prolonged in myocardial infarction patients (65.9+/-1.4 ms vs 91.2+/-2.3 ms, respectively, P<0.001). QT dispersion was negatively correlated to left ventricular ejection fraction (P<0.005). The ACE DD-genotype was associated with longer QT dispersion in myocardial infarction patients (103.0+/-4.6 ms vs 81.9+/-4.5 ms in the II group, P<0.001). This association was noted to be strong in multivariate analyses that included age, gender, ejection fraction, left ventricular end-diastolic diameter, medication, and heart rate. In contrast, no association between the ACE DD-genotype and QT dispersion was detected in healthy siblings of myocardial infarction patients. CONCLUSION: Thus, the ACE D-allele may be associated with increased QT dispersion in patients after myocardial infarction but not in healthy subjects. An interaction of myocardial damage and genetic predisposition that both enhance the activity of the renin angiotensin system may decrease the repolarization homogeneity of the heart.