Arsenic decreases rice yield, and inorganic grain As threatens human health; thus, strategies to decrease rice As are critically needed. Increased plant-available silica (Si) can decrease rice As, yet the source of Si matters. Rice husk, an underutilized and Si-rich byproduct of rice production that contains less labile C and an order of magnitude less As than rice straw, may be an economically viable Si resource to decrease rice As, yet the impact of rice husk incorporation on As in the rice-soil nexus has not been reported. This proof-of-concept study shows that rice husk incorporation to soil (1% w/w) decreases inorganic grain As by 25-50% without negatively affecting grain Cd, yield, or dissolved CH4 levels. Rice husk is a critical yet perhaps overlooked resource to improve soil quality through enhanced nutrient availability and attenuate human health risks through consumption of As-laden grain.
Microbial physiological processes are intimately involved in nutrient cycling. However, it remains unclear to what extent microbial diversity or community composition is important for determining the rates of ecosystem-scale functions. There are many examples of positive correlations between microbial diversity and ecosystem function, but how microbial communities ‘map' onto ecosystem functions remain unresolved. This uncertainty limits our ability to predict and manage crucial microbially mediated processes such as nutrient losses and greenhouse gas emissions. To overcome this challenge, we propose integrating traditional biodiversity–ecosystem function research with ideas from genotype–phenotype mapping in organisms. We identify two insights from genotype–phenotype mapping that could be useful for microbial biodiversity–ecosystem function studies: the concept of searching ‘agnostically' for markers of ecosystem function and controlling for population stratification to identify microorganisms uniquely associated with ecosystem function. We illustrate the potential for these approaches to elucidate microbial biodiversity–ecosystem function relationships by analysing a subset of published data measuring methane oxidation rates from tropical soils. We assert that combining the approaches of traditional biodiversity–ecosystem function research with ideas from genotype–phenotype mapping will generate novel hypotheses about how complex microbial communities drive ecosystem function and help scientists predict and manage changes to ecosystem functions resulting from human activities.
This article is part of the theme issue ‘Conceptual challenges in microbial community ecology’.
We have investigated 31 families segregation for Hunter Syndrome in order to advance our understanding of the genetics of this disease. The hair root test for the diagnosis of carriers of Hunter Syndrome was improved by the adoption of a new diagnostic index that distinguishes between carrier and normal females better than previous methods of analysis. One hundred and eleven female relatives of the affected children were tested by such procedures. This showed that seven out of 31 mothers were not carriers (22.6%), thus suggesting a small deficit of new mutation relative to the expectation that 33% of lethal, recessive alleles arise anew in a population at equilibrium at a sex-linked locus with equal mutation rates in male and female gametogenesis. The difference, however, is not statistically significant. The age of the parents of new mutants was slightly but significantly raised. Nevertheless, the independent increase in the age of the fathers of new female mutants was not statistically significant. Finally, a deficit of affected males was observed. This was significant and suggests the possibility of intrauterine loss of some affected males. Linkage analysis between the Hunter Syndrome locus, three polymorphisms in the Factor IX gene and the anonymous polymorphic probes 52A and DX13 showed that the Hunter locus is fairly closely linked to DX13, and hence distal to the Factor IX gene, while no linkage was observed with the 52A polymorphic site. The maximum lod score for the linkage between factor IX and the Hunter Syndrome locus was 0.424 at theta = 0.25; and that for the linkage between the Hunter Syndrome locus and DX13 was 3.01 at theta = 0.1.
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