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Defoliation and accelerating ripening are important measures for cotton mechanization, and judging the time of defoliation and accelerating the ripening and harvest of cotton relies heavily on the boll opening rate, making it a crucial factor to consider. The traditional methods of cotton opening rate determination are time-consuming, labor-intensive, destructive, and not suitable for a wide range of applications. In this study, the relationship between the change rate of the vegetation index obtained by the unmanned aerial vehicle multi-spectrum and the ground boll opening rate was established to realize rapid non-destructive testing of the boll opening rate. The normalized difference vegetation index (NDVI) and green normalized difference vegetation index (GNDVI) had good prediction ability for the boll opening rate. NDVI in the training set had an R2 of 0.912 and rRMSE of 15.387%, and the validation set performance had an R2 of 0.929 and rRMSE of 13.414%. GNDVI in the training set had an R2 of 0.901 and rRMSE of 16.318%, and the validation set performance had an R2 of 0.909 and rRMSE of 15.225%. The accuracies of the models based on GNDVI and NDVI were within the acceptable range. In terms of predictive models, random forests achieve the highest accuracy in predictions. Accurately predicting the cotton boll opening rate can support decision-making for harvest and harvest aid spray timing, as well as provide technical support for crop growth monitoring and precision agriculture. [ABSTRACT FROM AUTHOR]

RNA N 6 -methyladenosine (m 6 A) modification is involved in diverse biological processes. However, its role in spinal cord injury (SCI) is poorly understood. The m 6 A level increases in injured spinal cord, and METTL3, which is the core subunit of methyltransferase complex, is upregulated in reactive astrocytes and further stabilized by the USP1/UAF1 complex after SCI. The USP1/UAF1 complex specifically binds to and subsequently removes K48-linked ubiquitination of the METTL3 protein to maintain its stability after SCI. Moreover, conditional knockout of astrocytic METTL3 in both sexes of mice significantly suppressed reactive astrogliosis after SCI, thus resulting in widespread infiltration of inflammatory cells, aggravated neuronal loss, hampered axonal regeneration, and impaired functional recovery. Mechanistically, the YAP1 transcript was identified as a potential target of METTL3 in astrocytes. METTL3 could selectively methylate the 3'-UTR region of the YAP1 transcript, which subsequently maintains its stability in an IGF2BP2-dependent manner. In vivo , YAP1 overexpression by adeno-associated virus injection remarkably contributed to reactive astrogliosis and partly reversed the detrimental effects of METTL3 knockout on functional recovery after SCI. Furthermore, we found that the methyltransferase activity of METTL3 plays an essential role in reactive astrogliosis and motor repair, whereas METTL3 mutant without methyltransferase function failed to promote functional recovery after SCI. Our study reveals the previously unreported role of METTL3-mediated m 6 A modification in SCI and might provide a potential therapy for SCI. SIGNIFICANCE STATEMENT Spinal cord injury is a devastating trauma of the CNS involving motor and sensory impairments. However, epigenetic modification in spinal cord injury is still unclear. Here, we propose an m 6 A regulation effect of astrocytic METTL3 following spinal cord injury, and we further characterize its underlying mechanism, which might provide promising strategies for spinal cord injury treatment., Competing Interests: The authors declared no competing financial interests., (Copyright © 2023 the authors.)