Assessment of multiple herbicide protection seed treatments for seed-based restoration of native perennial bunchgrasses and sagebrush across multiple sites and years.

The invasion of exotic, annual plant species is a leading contributor to ecological degradation in drylands globally, and the use of pre-emergent herbicide to control these species is common. Pre-emergent herbicides pose challenges for seed-based restoration due to toxicity to the seeds of desired species. Herbicide protection (HP) technologies pose a potential solution by using activated carbon seed treatments to protect desirable seeds from herbicide exposure. In the sagebrush steppe ecosystem of North America, we used an adaptive small plot design over three planting years to test for effects on seeding outcomes (seedling density and size) of large and small multi-seed HP pellets, several single-seed HP coatings, and carbon banding treatments at geographically dispersed sites for several perennial bunchgrasses and the keystone perennial shrub, Wyoming big sagebrush. We also compared different methods of seed delivery and litter pre-seeding management. Seeding success was low overall, especially for sagebrush, and it was clear that other, often less predictable barriers to establishment than herbicide exposure, such as inadequate spring moisture, were strong drivers of seeding outcomes. Despite this, HP treatments were associated with higher seedling density than bare seed in multiple instances, most notably for grasses. The large HP pellet occasionally outperformed the small HP pellet, and several HP coatings performed similarly to the small pellet. Surprisingly, we did not see consistent negative effects of pre-emergent herbicide on unprotected bare seed. We conclude that HP seed treatments show some promise to improve seeding success in the presence of herbicide, but that consistent success will require further improvements to HP treatments as well as integration with other innovations and approaches.

ATP7B variant c.1934T > G p.Met645Arg causes Wilson disease by promoting exon 6 skipping.

Wilson disease is a recessive genetic disorder caused by pathogenic loss-of-function variants in the ATP7B gene. It is characterized by disrupted copper homeostasis resulting in liver disease and/or neurological abnormalities. The variant NM_000053.3:c.1934T > G (Met645Arg) has been reported as compound heterozygous, and is highly prevalent among Wilson disease patients of Spanish descent. Accordingly, it is classified as pathogenic by leading molecular diagnostic centers. However, functional studies suggest that the amino acid change does not alter protein function, leading one ClinVar submitter to question its pathogenicity. Here, we used a minigene system and gene-edited HepG2 cells to demonstrate that c.1934T > G causes ~70% skipping of exon 6. Exon 6 skipping results in frameshift and stop-gain, leading to loss of ATP7B function. The elucidation of the mechanistic effect for this variant resolves any doubt about its pathogenicity and enables the development of genetic medicines for restoring correct splicing.

No significant association between prenatal exposure poliovirus epidemics and psychosis.

OBJECTIVE: To examine the association between prenatal exposure to poliovirus infection and later development of schizophrenia or affective psychosis in a Southern Hemisphere psychiatric register. METHODS: We calculated rates of poliomyelitis cases per 10 000 background population and rates for schizophrenia(n = 6078) and affective psychosis (n = 3707)per 10 000 births for the period 1930-1964. Empirically weighted regression was used to measure the association between a given psychosis birth-rate and a poliomyelitis epidemic during gestation. RESULTS: There was no statistically significant association between exposure to a poliomyelitis epidemic during gestation and subsequent development of schizophrenia or affective psychosis. CONCLUSIONS: The lack of a consistent statistically significant association between poliovirus epidemics and schizophrenia suggests that either poliovirus may have a small effect which is only detectable with large data-sets and/or the effect may be modified by location. Further investigation of such inconsistencies may help elucidate candidate risk-modifying factors for schizophrenia.