A population genomics insight into the Mediterranean origins of wine yeast domestication

The domestication of the wine yeast Saccharomyces cerevisiae is thought to be contemporary with the development and expansion of viticulture along the Mediterranean basin. Until now, the unavailability of wild lineages prevented the identification of the closest wild relatives of wine yeasts. Here, we enlarge the collection of natural lineages and employ whole‐genome data of oak‐associated wild isolates to study a balanced number of anthropic and natural S. cerevisiae strains. We identified industrial variants and new geographically delimited populations, including a novel Mediterranean oak population. This population is the closest relative of the wine lineage as shown by a weak population structure and further supported by genomewide population analyses. A coalescent model considering partial isolation with asymmetrical migration, mostly from the wild group into the Wine group, and population growth, was found to be best supported by the data. Importantly, divergence time estimates between the two populations agree with historical evidence for winemaking. We show that three horizontally transmitted regions, previously described to contain genes relevant to wine fermentation, are present in the Wine group but not in the Mediterranean oak group. This represents a major discontinuity between the two populations and is likely to denote a domestication fingerprint in wine yeasts. Taken together, these results indicate that Mediterranean oaks harbour the wild genetic stock of domesticated wine yeasts.     

Seasonal nutrient fluxes variability of northern salt marshes: examples from the lower St. Lawrence Estuary

This study presents the tidal exchange of ammonium, nitrite + nitrate, phosphate and silicate between two salt marshes and adjacent estuarine waters. Marsh nutrient fluxes were evaluated for Pointe-au-Père and Pointe-aux-épinettes salt marshes, both located along the south shore of the lower St. Lawrence Estuary in Rimouski area (QC, Canada). Using nutrients field data, high precision bathymetric records and a hydrodynamic numerical model (MIKE21-NHD) forced with predicted tides, nutrients fluxes were estimated through salt marsh outlet cross-sections at four different periods of the year 2004 (March, May, July and November). Calculated marsh nutrient fluxes are discussed in relation with stream inputs, biotic and abiotic marsh processes and the incidence of sea ice cover. In both marshes, the results show the occurrence of year-round and seaward NH₄ ⁺ fluxes and landward NO₂ ⁻ + NO₃ ⁻ fluxes (ranging from 9.06 to 30.48 mg N day⁻¹ m⁻² and from −32.07 to −9.59 mg N day⁻¹ m⁻², respectively) as well as variable PO₄ ³⁻ and Si(OH)₄ fluxes (ranging from −3.73 to 6.34 mg P day⁻¹ m⁻² and from −29.19 to 21.91 mg Si day⁻¹ m⁻², respectively). These results suggest that NO₂ ⁻ + NO₃ ⁻ input to marshes can be a significant source of NH₄ ⁺ through dissimilatory nitrate reduction to ammonium (DNRA). This NH₄ ⁺, accumulating in marsh sediment rather than being removed through coupled nitrification–denitrification or biological assimilation, is exported toward estuarine waters. From average P and Si tidal fluxes analysis, both salt marshes act as a sink during high productivity period (May and July) and as a source, supplying estuarine water during low productivity period (November and March).     

Proteasomes and protein conjugation across domains of life

Like other energy-dependent proteases, proteasomes, which are found across the three domains of life, are self-compartmentalized and important in the early steps of proteolysis. Proteasomes degrade improperly synthesized, damaged or misfolded proteins and hydrolyse regulatory proteins that must be specifically removed or cleaved for cell signalling. In eukaryotes, proteins are typically targeted for proteasome-mediated destruction through polyubiquitylation, although ubiquitin-independent pathways also exist. Interestingly, actinobacteria and archaea also covalently attach small proteins (prokaryotic ubiquitin-like protein (Pup) and small archaeal modifier proteins (Samps), respectively) to certain proteins, and this may serve to target the modified proteins for degradation by proteasomes.     

(+)-ABA content and lipid deposition in interior spruce somatic embryos

Summary Interior spruce (Picea glauca engelmannii complex) somatic embryos grown on 48 μmol (±)-ABA per L over a period of 42 d without transfer underwent precocious germination by 49 d. Those transferred at 28 d to fresh medium with 48 μmol (±)-ABA continued embryo development until harvested at 56 d; the transfer at 28 d resulted in an increase in embryo lipid content after 42 d. Somatic embryos grown under this condition contained 181.4±41.2, 116.0±42.4, and 91.8±33.6 ng (+)-ABA per mg of lyophilized tissue at 42, 49, and 56 d, respectively. By comparison, embryos grown without the transfer at 28 d had 86.8±25.4 ng (+)-ABA per mg of lyophilized tissue at 42 d, just prior to precocious germination. After 3 weeks’ storage in a drying chamber under high humidity, the (+)-ABA content of 56-d-old transferred embryos decreased to 15.4 ± 4.4 ng (+)-ABA per mg of lyophilized tissue. The increased lipid content resulting from embryo transfer and the reduction in internal (+)-ABA content during storage are factors which will contribute to improved conversion of somatic embryos to plantlets.     

Functional significance of isoform diversification in the protocadherin gamma gene cluster

The mammalian Protocadherin (Pcdh) alpha, beta, and gamma gene clusters encode a large family of cadherin-like transmembrane proteins that are differentially expressed in individual neurons. The 22 isoforms of the Pcdhg gene cluster are diversified into A-, B-, and C-types, and the C-type isoforms differ from all other clustered Pcdhs in sequence and expression. Here, we show that mice lacking the three C-type isoforms are phenotypically indistinguishable from the Pcdhg null mutants, displaying virtually identical cellular and synaptic alterations resulting from neuronal apoptosis. By contrast, mice lacking three A-type isoforms exhibit no detectable phenotypes. Remarkably, however, genetically blocking apoptosis rescues the neonatal lethality of the C-type isoform knockouts, but not that of the Pcdhg null mutants. We conclude that the role of the Pcdhg gene cluster in neuronal survival is primarily, if not specifically, mediated by its C-type isoforms, whereas a separate role essential for postnatal development, likely in neuronal wiring, requires isoform diversity.