Ecosystem Consequences of Plant Genetic Divergence with Colonization of New Habitat

When plants colonize new habitats altered by natural or anthropogenic disturbances, those individuals may encounter biotic and abiotic conditions novel to the species, which can cause plant functional trait divergence. Over time, site-driven adaptation can give rise to population-level genetic variation, with consequences for plant community dynamics and ecosystem processes. We used a series of 3000-yr-old, lava-created forest fragments on the Island of Hawai`i to examine whether disturbance and subsequent colonization can lead to genetically differentiated populations, and where differentiation occurs, if there are ecosystem consequences of trait-driven changes. These fragments are dominated by a single tree species, Metrosideros polymorpha (Myrtaceae) or ʻohiʻa, which have been actively colonizing the surrounding lava flow created in 1858. To test our ideas about differentiation of genetically determined traits, we (1) created rooted cuttings of ʻohiʻa individuals sampled from fragment interiors and open lava sites, raised these individuals in a greenhouse, and then used these cuttings to create a common garden where plant growth was monitored for three years; and (2) assessed genetic variation and made QST/FST comparisons using microsatellite repeat markers. Results from the greenhouse showed quantitative trait divergence in plant height and pubescence across plants sampled from fragment interior and matrix sites. Results from the subsequent common garden study confirmed that the matrix environment can select for individuals with 9.1% less shoot production and 17.3% higher leaf pubescence. We found no difference in molecular genetic variation indicating gene flow among the populations. The strongest QST level was greater than the FST estimate, indicating sympatric genetic divergence in growth traits. Tree height was correlated with ecosystem properties such as soil carbon and nitrogen storage, soil carbon turnover rates, and soil phosphatase activity, indicating that selection for growth traits will influence structure, function, and dynamics of developing ecosystems. These data show that divergence can occur on centennial timescales of early colonization

Concentrations and size distributions of fungal bioaerosols in a municipal landfill

The object of this research was to study the behavior of fungal bioaerosols during a sampling period of 12 months (April 2015–April 2016), in each treatment stages of a landfill located in Atlántico Department, Colombia. The fungi bioaerosol samples were collected using a Six-Stage Viable Andersen Cascade Impactor - Thermo Fisher Scientific, a vacuum pump with a flow rate of 28.3 L/min–1, and ammeter KESTREL 4500 for the weather conditions. With the large amount of data obtained, a database was made in excel and analyzed using Statgraphics Centurion XVI software. The processing of data mining was carried out applying to a generalized linear regression model and Multifactorial ANOVA. Golden Surfer 11 program was used to stablish the distribution of temporal and spational mold airborne. The Variables: sampling campaign, stage, taxa, temperature and relative humidity presented a statistically significant correlation with the concentration P-value = 0. The concentrations of fungal bioaerosols varied considerably over the whole sampling period with average concentrations from 73.02 ± 26, 75 CFUs/m3 to 1830.38 ± 971.28 CFUs/m3. The fungal bioaerosols presented in both the coarse and fine fraction; but the fraction of 2.1–3.3 μm (stage 4) was the fraction of the dominant size in terms of higher concentration. According to the taxa identification, there was a higher prevalence of Aspergillus: the highest concentration corresponds to A. fumigatus, associated to toxins that may be cytotoxic [1, 2]

Bi-allelic JAM2 Variants Lead to Early-Onset Recessive Primary Familial Brain Calcification.

Primary familial brain calcification (PFBC) is a rare neurodegenerative disorder characterized by a combination of neurological, psychiatric, and cognitive decline associated with calcium deposition on brain imaging. To date, mutations in five genes have been linked to PFBC. However, more than 50% of individuals affected by PFBC have no molecular diagnosis. We report four unrelated families presenting with initial learning difficulties and seizures and later psychiatric symptoms, cerebellar ataxia, extrapyramidal signs, and extensive calcifications on brain imaging. Through a combination of homozygosity mapping and exome sequencing, we mapped this phenotype to chromosome 21q21.3 and identified bi-allelic variants in JAM2. JAM2 encodes for the junctional-adhesion-molecule-2, a key tight-junction protein in blood-brain-barrier permeability. We show that JAM2 variants lead to reduction of JAM2 mRNA expression and absence of JAM2 protein in patient's fibroblasts, consistent with a loss-of-function mechanism. We show that the human phenotype is replicated in the jam2 complete knockout mouse (jam2 KO). Furthermore, neuropathology of jam2 KO mouse showed prominent vacuolation in the cerebral cortex, thalamus, and cerebellum and particularly widespread vacuolation in the midbrain with reactive astrogliosis and neuronal density reduction. The regions of the human brain affected on neuroimaging are similar to the affected brain areas in the myorg PFBC null mouse. Along with JAM3 and OCLN, JAM2 is the third tight-junction gene in which bi-allelic variants are associated with brain calcification, suggesting that defective cell-to-cell adhesion and dysfunction of the movement of solutes through the paracellular spaces in the neurovascular unit is a key mechanism in CNS calcification

Memristive and neuromorphic behavior in a Li x CoO 2 nanobattery

International audienceThe phenomenon of resistive switching (RS), which was initially linked to non-volatile resistive memory applications, has recently also been associated with the concept of memristors, whose adjustable multilevel resistance characteristics open up unforeseen perspectives in cognitive computing. Herein, we demonstrate that the resistance states of Li(x)CoO2 thin film-based metal-insulator-metal (MIM) solid-state cells can be tuned by sequential programming voltage pulses, and that these resistance states are dramatically dependent on the pulses input rate, hence emulating biological synapse plasticity. In addition, we identify the underlying electrochemical processes of RS in our MIM cells, which also reveal a nanobattery-like behavior, leading to the generation of electrical signals that bring an unprecedented new dimension to the connection between memristors and neuromorphic systems. Therefore, these LixCoO2-based MIM devices allow for a combination of possibilities, offering new perspectives of usage in nanoelectronics and bio-inspired neuromorphic circuits

Multisensory and Motor Representations in Rat Oral Somatosensory Cortex

Abstract In mammals, a complex array of oral sensors assess the taste, temperature and haptic properties of food. Although the representation of taste has been extensively studied in the gustatory cortex, it is unclear how the somatosensory cortex encodes information about the properties of oral stimuli. Moreover, it is poorly understood how different oral sensory modalities are integrated and how sensory responses are translated into oral motor actions. To investigate whether oral somatosensory cortex processes food-related sensations and movements, we performed in vivo whole-cell recordings and motor mapping experiments in rats. Neurons in oral somatosensory cortex showed robust post-synaptic and sparse action potential responses to air puffs. Membrane potential showed that cold water evoked larger responses than room temperature or hot water. Most neurons showed no clear tuning of responses to bitter, sweet and neutral gustatory stimuli. Finally, motor mapping experiments with histological verification revealed an initiation of movements related to food consumption behavior, such as jaw opening and tongue protrusions. We conclude that somatosensory cortex: (i) provides a representation of the temperature of oral stimuli, (ii) does not systematically encode taste information and (iii) influences orofacial movements related to food consummatory behavior

PDXK mutations cause polyneuropathy responsive to pyridoxal 5'-phosphate supplementation.

OBJECTIVE: To identify disease-causing variants in autosomal recessive axonal polyneuropathy with optic atrophy and provide targeted replacement therapy. METHODS: We performed genome-wide sequencing, homozygosity mapping, and segregation analysis for novel disease-causing gene discovery. We used circular dichroism to show secondary structure changes and isothermal titration calorimetry to investigate the impact of variants on adenosine triphosphate (ATP) binding. Pathogenicity was further supported by enzymatic assays and mass spectroscopy on recombinant protein, patient-derived fibroblasts, plasma, and erythrocytes. Response to supplementation was measured with clinical validated rating scales, electrophysiology, and biochemical quantification. RESULTS: We identified biallelic mutations in PDXK in 5 individuals from 2 unrelated families with primary axonal polyneuropathy and optic atrophy. The natural history of this disorder suggests that untreated, affected individuals become wheelchair-bound and blind. We identified conformational rearrangement in the mutant enzyme around the ATP-binding pocket. Low PDXK ATP binding resulted in decreased erythrocyte PDXK activity and low pyridoxal 5'-phosphate (PLP) concentrations. We rescued the clinical and biochemical profile with PLP supplementation in 1 family, improvement in power, pain, and fatigue contributing to patients regaining their ability to walk independently during the first year of PLP normalization. INTERPRETATION: We show that mutations in PDXK cause autosomal recessive axonal peripheral polyneuropathy leading to disease via reduced PDXK enzymatic activity and low PLP. We show that the biochemical profile can be rescued with PLP supplementation associated with clinical improvement. As B6 is a cofactor in diverse essential biological pathways, our findings may have direct implications for neuropathies of unknown etiology characterized by reduced PLP levels. ANN NEUROL 2019;86:225-240

Competition and Prosociality: A Field Experiment in Ghana

Competitive bonuses are commonly used to promote higher productivity in the workplace. Yet, these types of incentives could have negative spillovers on coworkers' prosocial behavior in subsequent tasks. To investigate this question, we conduct a lab-in-the-eld experiment in Ghana. In a between-subjects design, participants complete a real-eort task under a competitive, threshold, or random payment while holding payment dierentials constant across treatments. Before and after, we measure prosociality through a public goods and a social value orientation game. Competition reduces prosociality when the dispersion of payments is high. However, when there is less at stake, competition does not aect prosociality

Disentangling balance impairments in spinal and bulbar muscular atrophy

Spinal and bulbar muscular atrophy (Kennedy's disease) has been associated with balance dysfunction and falls. However, postural control has not been studied quantitatively. Here, we quantified upright stance and aimed to disentangle the role of vestibular, proprioceptive and oculomotor deficits. Static balance was assessed in Kennedy patients (n = 7) during quiet stance on a force platform under different visual and proprioceptive feedback conditions. Vestibular function was assessed with the video head impulse test. Sural nerve neurography was employed to evaluate the severity of peripheral neuropathy. Also, horizontal saccades were recorded and quantified by the main sequence relationship. Posturographic analyses revealed significantly increased body sway, more pronounced in conditions with closed eyes, which was also reflected in the calculated Romberg indices. Horizontal vestibulo-ocular reflex gains were normal, i.e. > 0.75. In contrast, compound sensory nerve action potentials were markedly decreased in all patients (mean = 2.4 μV). Two patients showed slow saccades with increased exponential main sequence constants. We conclude that Kennedy patients exhibit severe deficits in quiet stance. Postural instability is greatest in conditions of absent vision with reduced proprioception being the main determinant of unsteadiness. Some patients show slowed saccadic eye movements suggesting a nuclear abducens neuronopathy. © 2019 Elsevier B.V