Phenotypic noise and the cost of complexity

Experimental studies demonstrate the existence of phenotypic diversity despite constant genotype and environment. Theoretical models based on a single phenotypic character predict that during an adaptation event, phenotypic noise should be positively selected far from the fitness optimum because it increases the fitness of the genotype, and then be selected against when the population reaches the optimum. It is suggested that because of this fitness gain, phenotypic noise should promote adaptive evolution. However, it is unclear how the selective advantage of phenotypic noise is linked to the rate of evolution, and whether any advantage would hold for more realistic, multidimensional phenotypes. Indeed, complex organisms suffer a cost of complexity, where beneficial mutations become rarer as the number of phenotypic characters increases. Using a quantitative genetics approach, we first show that for a one-dimensional phenotype, phenotypic noise promotes adaptive evolution on plateaus of positive fitness, independently from the direct selective advantage on fitness. Second, we show that for multidimensional phenotypes, phenotypic noise evolves to a low-dimensional configuration, with elevated noise in the direction of the fitness optimum. Such a dimensionality reduction of the phenotypic noise promotes adaptive evolution and numerical simulations show that it reduces the cost of complexity.     

Indirect N2O emissions from shallow groundwater in an agricultural catchment (Seine Basin, France)

Production and accumulation of nitrous oxide (N₂O), a major greenhouse gas, in shallow groundwater might contribute to indirect N₂O emissions to the atmosphere (e.g., when groundwater flows into a stream or a river). The Intergovernmental Panel on Climate Change (IPCC) has attributed an emission factor (EF_5g) for N₂O, associated with nitrate leaching in groundwater and drainage ditches—0.0025 (corresponding to 0.25% of N leached which is emitted as N₂O)—although this is the subject of considerable uncertainty. We investigated and quantified the transport and fate of nitrate (NO₃ ^?) and dissolved nitrous oxide from crop fields to groundwater and surface water over a 2-year period (monitoring from April 2008 to April 2010) in a transect from a plateau to the river with three piezometers. In groundwater, nitrate concentrations ranged from 1.0 to 22.7 mg NO₃ ^?–N l^?1 (from 2.8 to 37.5 mg NO₃ ^?–N l^?1 in the river) and dissolved N₂O from 0.2 to 101.0 μg N₂O–N l^?1 (and from 0.2 to 2.9 μg N₂O–N l^?1 in the river). From these measurements, we estimated an emission factor of EF_5g = 0.0026 (similar to the value currently used by the IPCC) and an annual indirect N₂O flux from groundwater of 0.035 kg N₂O–N ha^?1 year^?1, i.e., 1.8% of the previously measured direct N₂O flux from agricultural soils.     

Protist Biodiversity and Biogeography in Lakes From Four Brazilian River–Floodplain Systems

The biodiversity and biogeography of protists inhabiting many ecosystems have been intensely studied using different sequencing approaches, but tropical ecosystems are relatively under‐studied. Here, we sampled planktonic waters from 32 lakes associated with four different river–floodplains systems in Brazil, and sequenced the DNA using a metabarcoding approach with general eukaryotic primers. The lakes were dominated by the largely free‐living Discoba (mostly the Euglenida), Ciliophora, and Ochrophyta. There was low community similarity between lakes even within the same river–floodplain. The protists inhabiting these floodplain systems comprise part of the large and relatively undiscovered diversity in the tropics.     

PP1-mediated moesin dephosphorylation couples polar relaxation to mitotic exit

Animal cells undergo dramatic actin-dependent changes in shape as they progress through mitosis; they round up upon mitotic entry and elongate during chromosome segregation before dividing into two [1-3]. Moesin, the sole Drosophila ERM-family protein [4], plays a critical role in this process, through the construction of a stiff, rounded metaphase cortex [5-7]. At mitotic exit, this rigid cortex must be dismantled to allow for anaphase elongation and cytokinesis through the loss of the active pool of phospho-Thr559moesin from cell poles. Here, in an RNA interference (RNAi) screen for phosphatases involved in the temporal and spatial control of moesin, we identify PP1-87B RNAi as having elevated p-moesin levels and reduced cortical compliance. In mitosis, RNAi-induced depletion of PP1-87B or depletion of a conserved noncatalytic PP1 phosphatase subunit Sds22 leads to defects in p-moesin clearance from cell poles at anaphase, a delay in anaphase elongation, together with defects in bipolar anaphase relaxation and cytokinesis. Importantly, similar cortical defects are seen at anaphase following the expression of a constitutively active, phosphomimetic version of moesin. These data reveal a new role for the PP1-87B/Sds22 phosphatase, an important regulator of the metaphase-anaphase transition, in coupling moesin-dependent cell shape changes to mitotic exit.     

Rasl11b knock down in zebrafish suppresses one-eyed-pinhead mutant phenotype

The EGF-CFC factor Oep/Cripto1/Frl1 has been implicated in embryogenesis and several human cancers. During vertebrate development, Oep/Cripto1/Frl1 has been shown to act as an essential coreceptor in the TGFbeta/Nodal pathway, which is crucial for germ layer formation. Although studies in cell cultures suggest that Oep/Cripto1/Frl1 is also implicated in other pathways, in vivo it is solely regarded as a Nodal coreceptor. We have found that Rasl11b, a small GTPase belonging to a Ras subfamily of putative tumor suppressor genes, modulates Oep function in zebrafish independently of the Nodal pathway. rasl11b down regulation partially rescues endodermal and prechordal plate defects of zygotic oep(-/-) mutants (Zoep). Rasl11b inhibitory action was only observed in oep-deficient backgrounds, suggesting that normal oep expression prevents Rasl11b function. Surprisingly, rasl11b down regulation does not rescue mesendodermal defects in other Nodal pathway mutants, nor does it influence the phosphorylation state of the downstream effector Smad2. Thus, Rasl11b modifies the effect of Oep on mesendoderm development independently of the main known Oep output: the Nodal signaling pathway. This data suggests a new branch of Oep signaling that has implications for germ layer development, as well as for studies of Oep/Frl1/Cripto1 dysfunction, such as that found in tumors.     

Benzo[a]pyrene, aflatoxine B₁ and acetaldehyde mutational patterns in TP53 gene using a functional assay: relevance to human cancer aetiology

Mutations in the TP53 gene are the most common alterations in human tumours. TP53 mutational patterns have sometimes been linked to carcinogen exposure. In hepatocellular carcinoma, a specific G>T transversion on codon 249 is classically described as a fingerprint of aflatoxin B(1) exposure. Likewise G>T transversions in codons 157 and 158 have been related to tobacco exposure in human lung cancers. However, controversies remain about the interpretation of TP53 mutational pattern in tumours as the fingerprint of genotoxin exposure. By using a functional assay, the Functional Analysis of Separated Alleles in Yeast (FASAY), the present study depicts the mutational pattern of TP53 in normal human fibroblasts after in vitro exposure to well-known carcinogens: benzo[a]pyrene, aflatoxin B(1) and acetaldehyde. These in vitro patterns of mutations were then compared to those found in human tumours by using the IARC database of TP53 mutations. The results show that the TP53 mutational patterns found in human tumours can be only partly ascribed to genotoxin exposure. A complex interplay between the functional impact of the mutations on p53 phenotype and the cancer natural history may affect these patterns. However, our results strongly support that genotoxins exposure plays a major role in the aetiology of the considered cancers.     

Mixing Languages during Learning? Testing the One Subject—One Language Rule

In bilingual communities, mixing languages is avoided in formal schooling: even if two languages are used on a daily basis for teaching, only one language is used to teach each given academic subject. This tenet known as the one subject-one language rule avoids mixing languages in formal schooling because it may hinder learning. The aim of this study was to test the scientific ground of this assumption by investigating the consequences of acquiring new concepts using a method in which two languages are mixed as compared to a purely monolingual method. Native balanced bilingual speakers of Basque and Spanish—adults (Experiment 1) and children (Experiment 2)—learnt new concepts by associating two different features to novel objects. Half of the participants completed the learning process in a multilingual context (one feature was described in Basque and the other one in Spanish); while the other half completed the learning phase in a purely monolingual context (both features were described in Spanish). Different measures of learning were taken, as well as direct and indirect indicators of concept consolidation. We found no evidence in favor of the non-mixing method when comparing the results of two groups in either experiment, and thus failed to give scientific support for the educational premise of the one subject—one language rule.     

Mammalian 8-oxoguanine DNA glycosylase 1 incises 8-oxoadenine opposite cytosine in nuclei and mitochondria,while a different glycosylase incises 8-oxoadenine opposite guanine in nuclei

Cells are continuously exposed to oxidative species, which cause several types of oxidative DNA lesions. Repair of some of these lesions has been well characterized but little is known about the repair of many DNA lesions. The oxidized adenine base, 7,8-dihydro-8-oxoadenine (8-oxoA), is a relatively common DNA lesion, which is believed to be mutagenic in mammalian cells. This study investigates repair of 8-oxoA in nuclear and mitochondrial mammalian extracts. In nuclei, 8-oxoA:C and 8-oxoA:G base pairs are recognized and cleaved; in contrast, only 8-oxoA:C base pairs are cleaved in mitochondria. High stability of the DNA helix increased the efficiency of incision of 8-oxoA, and the efficiency decreased at DNA bends and condensed regions of the helix. Using liver extracts from mice knocked out for 8-oxoguanine DNA glycosylase 1 (OGG1), we demonstrated that OGG1 is the only glycosylase that incises 8-oxoA, when base-paired with cytosine in mitochondria and nuclei, but a different enzyme incises 8-oxoA when base-paired with guanine in the nucleus. Consistent with this result, a covalent DNA-protein complex was trapped using purified human OGG1 or human nuclear or mitochondrial extracts with a DNA substrate containing an 8-oxoA:C base pair.