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Bates, T.

Publications and source records attributed to Bates, T..

3 recordsLinked to original sources

Warming winters, changing springs: cold hardiness dynamics predict budbreak and associated low temperature threats on an intercontinental scale

Temperate woody perennial plants form buds that develop into leaves or flowers that emerge in the following growth season. To survive winter, dormant buds must attain cold hardiness, and timely lose it in spring to break bud while avoiding damage from low temperatures and late frosts. Here, we use a process-based model to predict bud cold hardiness of three grapevine varieties (V. vinifera Cabernet-Sauvignon and Riesling, and V. hybrid Concord) from historical temperature records of eight different locations in North America and Europe (n=329). Based on those predictions, and thresholds of cold hardiness at budbreak from literature, timing of budbreak was extracted. Despite the model being untrained to budbreak data, the cold hardiness model resulted in good predictions (RMSE=7.3d) that were further improved based on expected delays from cold damage (RMSE=7.2d). Both increasing and decreasing trends in freeze damage risk were predicted with increasing temperature, depending on the range of mean dormant season temperature (MDST; 1 Nov-30 Apr) in each location. Predictions in timing of spring phenology in relation to MDST also showed warming to advance (MDST<10{degrees}C) or delay (MDST>10{degrees}C) budbreak. Cold hardiness dynamics represents an advancement in phenological modeling that provides information for the entirety of the dormant season, as well as budbreak.

plant biology↗

Assessing the capacity of high-resolution commercial satellite imagery for grapevine downy mildew detection and surveillance in New York state

Grapevine downy mildew (GDM), caused by the oomycete Plasmopara viticola, can cause 100% yield loss and vine death under conducive conditions. Growers currently rely on frequent fungicide applications for control, but this practice has led to widespread resistance. Rapid remote detection and surveillance of GDM outbreaks would enable precision pesticide applications to target effective but resistance-prone fungicides where and when most needed, while relying on less resistance-prone protectants elsewhere. High resolution commercial satellite platforms offer the opportunity to track rapidly spreading diseases like GDM over large, heterogeneous fields. Here, we investigate the capacity of PlanetScope (3 m) and SkySat (50 cm) imagery for season-long GDM detection and surveillance. A team of trained scouts rated GDM severity and incidence in two acres of Chardonnay grapevines in Geneva, NY, USA in June-August of 2020, 2021, and 2022. Satellite imagery acquired within 72 hours of scouting was processed to extract single-band reflectance and vegetation indices (VIs). Random forest models trained on spectral bands and VIs derived from both image datasets could classify areas of high and low GDM incidence and severity with maximum accuracies of 0.88 (SkySat) and 0.94 (PlanetScope). However, we do not observe significant differences between VIs of high and low damage classes until late July-early August. We identify cloud cover, image co-registration, and low spectral resolution as key challenges to operationalizing satellite-based GDM surveillance. This work establishes the capacity of spaceborne multispectral sensors to detect late-stage GDM and outlines steps towards incorporating satellite remote sensing in grapevine disease surveillance systems.

plant biology↗

Pax9 is required for cardiovascular development and interacts with Tbx1 in the pharyngeal endoderm to control 4th pharyngeal arch artery morphogenesis.

Developmental defects affecting the heart and aortic arch arteries are a key phenotype observed in DiGeorge syndrome patients and are caused by a microdeletion on chromosome 22q11. Heterozygosity of TBX1, one of the deleted genes, is expressed throughout the pharyngeal arches and is considered a key component for the arch artery defects. Pax9 is expressed in the pharyngeal endoderm and is downregulated in Tbx1 mutant mice. We show here that Pax9 deficient mice are born with complex cardiovascular malformations affecting the outflow tract and aortic arch arteries with failure of the 3rd and 4th pharyngeal arch arteries to form correctly. Transcriptome analysis indicated that Pax9 and Tbx1 may function together, and mice double heterozygous for Tbx1/Pax9 presented with a significantly increased incidence of interrupted aortic arch when compared to Tbx1 heterozygous mice. Using a novel Pax9Cre allele we demonstrated that the site of this Tbx1-Pax9 genetic interaction is in the pharyngeal endoderm, therefore revealing that a Tbx1/Pax9-controlled signalling mechanism emanating from the pharyngeal endoderm is required for critical tissue interactions during normal morphogenesis of the pharyngeal arch artery system.\n\nSummary statementPax9 is required for outflow tract and aortic arch development, and functions together with Tbx1 in the pharyngeal endoderm for 4th arch artery formation.

developmental biology↗