Sesame (Sesamum indicum) Response to Postemergencedirected Herbicide Applications

Field studies were conducted from 2006 to 2010 under weed-free conditions in south Texas and in the Texas High Plains to determine sesame tolerance to applied postemergence-directed herbicides. Injury was greatest when herbicides were applied to 15 cm of the main stem compared to herbicide applications made to 5 cm of the main stem height. Glyphosate at 0.84 kg ae/ha and pyrithiobac-sodium at 0.07 kg ai/ha resulted in the greatest sesame stunting (28–90%) when applied up to 15 cm main stem height, while carfentrazone-ethyl, flumioxazin, and imazethapyr caused greatest injury when applied to 5 cm of the main stem. When glyphosate was applied up to 5 cm main stem height, sesame injury was 20% or less. Glyphosate applied up to the 15 cm stem height and pyrithiobac-sodium applied 5 and 15 cm stem height consistently reduced sesame yield when compared with the nontreated control. Acetochlor, diuron, fluometuron, and prometryn did not cause any sesame stunting. Carfentrazone-ethyl, diuron, flumioxazin, imazethapyr, propazine, pyraflufen-ethyl, linuron, and linuron plus diuron reduced sesame yield in at least one year in south Texas

Breeding history for shattering trait in sesame: classic to genomic approach

Sesame is an important oilseed crop that has high oil and protein content and unique antioxidant lignans. Capsule shattering at harvest is one of the most important problems affecting sesame production, with seed losses of up to 50%, making the crop unsuitable for mechanized harvesting. This paper provides an overview of breeding approaches addressing the capsule shattering trait in sesame and gives an outlook about the future perspectives of improvement for this trait. Sesame research has proceeded along the following parallel tracks: breeding for additional shatter resistance for manual harvest, breeding for mechanized harvest, and using molecular biology to improve the shatter resistance trait. In the future, genes controlling the shattering trait should be studied with techniques like RNA interference (RNAi), site-oriented mutagenesis, and gene editing with zinc finger nucleases (ZFNs) or CRISPR/Cas9, to develop new sesame varieties with capsules suitable for fully mechanized harvest

Response of Sesame to Selected Herbicides Applied Early in the Growing Season

Growth chamber experiments were conducted to evaluate the response of sesame to PRE and POST applications of soil residual herbicides. PRE applications of acetochlor and S-metolachlor at 1.26 and 1.43 kg ai·ha−1 showed little or no sesame injury (0 to 1%) 4 wks after herbicide treatments (WAT). POST treatments of acetochlor and trifluralin made 3 wks after planting (WAP) resulted in greater sesame injury (40%) compared to applications at bloom (18%). Field studies were conducted in Texas and Oklahoma during the 2014 and 2015 growing seasons to determine sesame response to clethodim, diuron, fluometuron, ethalfluralin, quizalofop-P, pendimethalin, pyroxasulfone, trifluralin, and trifloxysulfuron-sodium applied 2, 3, or 4 weeks after planting (WAP). Late-season sesame injury with the dinitroaniline herbicides consisted of a proliferation of primary branching at the upper nodes of the sesame plant (in the shape/form of a broom). Ethalfluralin and trifluralin caused more “brooming” effect than pendimethalin. Some yield reductions were noted with the dinitroaniline herbicides. Trifloxysulfuron-sodium caused the greatest injury (up to 97%) and resulted in yield reductions from the untreated check. Early-season diuron injury (leaf chlorosis and necrosis) decreased as application timing was delayed, and late-season injury was virtually nonexistent with only slight chlorosis (<4%) still apparent on the lower leaves. Sesame yield was not consistently affected by the diuron treatments. Fluometuron caused early-season injury (stunting/chlorosis), and a reduction of yield was observed at one location. Pyroxasulfone applied 2 WAP caused up to 25% sesame injury (stunting) but did not result in a yield reduction. Quizalofop-P caused slight injury (<5%) and no reduction in yield

Mapping the human genetic architecture of COVID-19

The genetic make-up of an individual contributes to the susceptibility and response to viral infection. Although environmental, clinical and social factors have a role in the chance of exposure to SARS-CoV-2 and the severity of COVID-191,2, host genetics may also be important. Identifying host-specific genetic factors may reveal biological mechanisms of therapeutic relevance and clarify causal relationships of modifiable environmental risk factors for SARS-CoV-2 infection and outcomes. We formed a global network of researchers to investigate the role of human genetics in SARS-CoV-2 infection and COVID-19 severity. Here we describe the results of three genome-wide association meta-analyses that consist of up to 49,562 patients with COVID-19 from 46 studies across 19 countries. We report 13 genome-wide significant loci that are associated with SARS-CoV-2 infection or severe manifestations of COVID-19. Several of these loci correspond to previously documented associations to lung or autoimmune and inflammatory diseases3–7. They also represent potentially actionable mechanisms in response to infection. Mendelian randomization analyses support a causal role for smoking and body-mass index for severe COVID-19 although not for type II diabetes. The identification of novel host genetic factors associated with COVID-19 was made possible by the community of human genetics researchers coming together to prioritize the sharing of data, results, resources and analytical frameworks. This working model of international collaboration underscores what is possible for future genetic discoveries in emerging pandemics, or indeed for any complex human disease