The differential assimilation of nitrogen fertilizer compounds by soil microorganisms.

The differential soil microbial assimilation of common nitrogen (N) fertilizer compounds into the soil organic N pool is revealed using novel compound-specific amino acid (AA) 15N-stable isotope probing. The incorporation of fertilizer 15N into individual AAs reflected the known biochemistry of N assimilation-e.g. 15N-labelled ammonium (15NH4+) was assimilated most quickly and to the greatest extent into glutamate. A maximum of 12.9% of applied 15NH4+, or 11.7% of 'retained' 15NH4+ (remaining in the soil) was assimilated into the total hydrolysable AA pool in the Rowden Moor soil. Incorporation was lowest in the Rowden Moor 15N-labelled nitrate (15NO3-) treatment, at 1.7% of applied 15N or 1.6% of retained 15N. Incorporation in the 15NH4+ and 15NO3- treatments in the Winterbourne Abbas soil, and the 15N-urea treatment in both soils was between 4.4% and 6.5% of applied 15N or 5.2% and 6.4% of retained 15N. This represents a key step in greater comprehension of the microbially mediated transformations of fertilizer N to organic N and contributes to a more complete picture of soil N-cycling. The approach also mechanistically links theoretical/pure culture derived biochemical expectations and bulk level fertilizer immobilization studies, bridging these different scales of understanding.

Hourly potential evapotranspiration at 0.1° resolution for the global land surface from 1981-present.

Challenges exist for assessing the impacts of climate and climate change on the hydrological cycle on local and regional scales, and in turn on water resources, food, energy, and natural hazards. Potential evapotranspiration (PET) represents atmospheric demand for water, which is required at high spatial and temporal resolutions to compute actual evapotranspiration and thus close the water balance near the land surface for many such applications, but there are currently no available high-resolution datasets of PET. Here we develop an hourly PET dataset (hPET) for the global land surface at 0.1° spatial resolution, based on output from the recently developed ERA5-Land reanalysis dataset, over the period 1981 to present. We show how hPET compares to other available global PET datasets, over common spatiotemporal resolutions and time frames, with respect to spatial patterns of climatology and seasonal variations for selected humid and arid locations across the globe. We provide the data for users to employ for multiple applications to explore diurnal and seasonal variations in evaporative demand for water.

Aridity is expressed in river topography globally.

It has long been suggested that climate shapes land surface topography through interactions between rainfall, runoff and erosion in drainage basins1-4. The longitudinal profile of a river (elevation versus distance downstream) is a key morphological attribute that reflects the history of drainage basin evolution, so its form should be diagnostic of the regional expression of climate and its interaction with the land surface5-9. However, both detecting climatic signatures in longitudinal profiles and deciphering the climatic mechanisms of their development have been challenging, owing to the lack of relevant global data and to the variable effects of tectonics, lithology, land surface properties and human activities10,11. Here we present a global dataset of 333,502 river longitudinal profiles, and use it to explore differences in overall profile shape (concavity) across climate zones. We show that river profiles are systematically straighter with increasing aridity. Through simple numerical modelling, we demonstrate that these global patterns in longitudinal profile shape can be explained by hydrological controls that reflect rainfall-runoff regimes in different climate zones. The most important of these is the downstream rate of change in streamflow, independent of the area of the drainage basin. Our results illustrate that river topography expresses a signature of aridity, suggesting that climate is a first-order control on the evolution of the drainage basin.

Live birth following the first mutation specific pre-implantation genetic diagnosis for haemophilia A.

Haemophilia A is an X-linked, recessive, inherited bleeding disorder which affects 1 in 5000 males born worldwide. It is caused by mutations in the FactorVIII (F8) gene on chromosome Xq28. We describe for the first time two mutation specific, single cell protocols for pre-implantation genetic diagnosis (PGD) of haemophilia. A that enable the selection of both male and female unaffected embryos. This approach offers an alternative to sexing, frequently used for X-linked disorders, that results in the discarding of all male embryos including the 50% that would have been normal. Two families with a history of severe haemophilia. A requested carrier diagnosis and subsequently proceeded to PGD. The mutation in family 1 is a single nucleotide substitution c.5953C > T, R1966X in exon 18 and in family 2, c.5122C > T, R1689C in exon 14 of the F8 gene. Amplification efficiency was compared between distilled water and SDS/proteinase K cell lysis (98.0%, 96/98 and 80%, 112/140 respectively) using 238 single lymphocytes. Blastomeres from spare IVF cleavage-stage embryos donated for research showed amplification efficiencies of 83.3% (45/54) for the R1966X and 92.9% (13/14) for the R1689C mutations. The rate of allele dropout (ADO) on heterozygous lymphocytes was 1.1% (1/93) for R1966X and 5.94% (6/101) for R1689C mutations. A single PGD treatment cycle for family 1 resulted in two embryos for transfer but these failed to implant. However, with family 2, two embryos were transferred to the uterus on day 4 resulting in a successful singleton pregnancy and subsequent live birth of a normal non-carrier female.

A common ancestral glycoprotein (GP) 9 1828A>G (Asn45Ser) gene mutation occurring in European families from Australia and Northern Europe with Bernard-Soulier Syndrome (BSS).

Bernard-Soulier syndrome (BSS) is an extremely rare hereditary bleeding disorder, caused by mutations occurring in the Glycoprotein (GP) Ibalpha, GPIbbeta and GP9 genes that encode for the corresponding subunits of platelet GPIb-V-IX adhesion receptor complex. BSS has been reported in many populations, mostly behaving in an autosomal-recessive manner.While the great majority of BSS mutations are unique to a single individual or family, the GP9 1828A>G Asn45Ser mutation, which we have identified in an undocumented Australian Caucasian, has already been reported in multiple unrelated Caucasian families from various Northern and Central European countries. Haplotype analysis of 19 BSS patients from 15 unrelated Northern European families (including 2 compound heterozygote siblings from a British family previously published, and 17 1828A>G Asn45Ser homozygotes), showed that 14 of these BSS patients from 11 of the 1828A>G Asn45Ser homozygote families share a common haplotype at the chromosomal region 3' to the GP9 gene. Hence, the results suggest that the GP9 1828A>GAsn45Ser mutation in these families is ancient, and its frequent emergence in the European population is the result of a founder effect rather than recurrent mutational events. Association of the 1828A>G Asn45Ser mutation with variant haplotypes in 4 other Northern European BSS families raised the possibility of a second founder event, or rare recombinations in these families. Additional members from these 'atypical' lineages would need to be screened to resolve this question.