Towards Robust Plant Disease Diagnosis with Hard-sample Re-mining Strategy

With rich annotation information, object detection-based automated plant disease diagnosis systems (e.g., YOLO-based systems) often provide advantages over classification-based systems (e.g., EfficientNet-based), such as the ability to detect disease locations and superior classification performance. One drawback of these detection systems is dealing with unannotated healthy data with no real symptoms present. In practice, healthy plant data appear to be very similar to many disease data. Thus, those models often produce mis-detected boxes on healthy images. In addition, labeling new data for detection models is typically time-consuming. Hard-sample mining (HSM) is a common technique for re-training a model by using the mis-detected boxes as new training samples. However, blindly selecting an arbitrary amount of hard-sample for re-training will result in the degradation of diagnostic performance for other diseases due to the high similarity between disease and healthy data. In this paper, we propose a simple but effective training strategy called hard-sample re-mining (HSReM), which is designed to enhance the diagnostic performance of healthy data and simultaneously improve the performance of disease data by strategically selecting hard-sample training images at an appropriate level. Experiments based on two practical in-field eight-class cucumber and ten-class tomato datasets (42.7K and 35.6K images) show that our HSReM training strategy leads to a substantial improvement in the overall diagnostic performance on large-scale unseen data. Specifically, the object detection model trained using the HSReM strategy not only achieved superior results as compared to the classification-based state-of-the-art EfficientNetV2-Large model and the original object detection model, but also outperformed the model using the HSM strategy

Significantly low level of small RNA accumulation derived from an encapsidated mycovirus with dsRNA genome

AbstractThe role of RNA silencing as an antiviral defence has been well elucidated in plants and invertebrates, but not in filamentous fungi. We have previously determined the complete genome sequence of Magnaporthe oryzae virus 2 (MoV2), a dsRNA virus that infects the rice blast fungus Magnaporthe oryzae. In this study, we detected small interfering RNAs (siRNAs) from both positive- and negative-strand MoV2 viral RNA, suggesting that the RNA silencing machinery in M. oryzae functions against the mycovirus. Cloning and characterisation of MoV2 siRNAs indicated that, in MoV2, the ratio of virus-derived siRNAs to total small RNA is significantly lower than that in either plant viruses or Cryphonectria hypovirus 1 (CHV1), another mycovirus. Nevertheless, any MoV2-encoded proteins did not exhibit RNA silencing suppressor activity in both the plant and fungal systems. Our study suggests the existence of a novel viral strategy employed to evade host RNA silencing

Osh proteins regulate COPII-mediated vesicular transport of ceramide from the endoplasmic reticulum in budding yeast

Lipids synthesized at the endoplasmic reticulum (ER) are delivered to the Golgi by vesicular and non-vesicular pathways. ER-to-Golgi transport is crucial for maintaining the different membrane lipid composition and identities of organelles. Despite their importance, mechanisms regulating transport remain elusive. Here we report that in yeast coat protein complex II (COPII) vesicle-mediated transport of ceramide from the ER to the Golgi requires oxysterol-binding protein homologs, Osh proteins, which have been implicated in lipid homeostasis. Because Osh proteins are not required to transport proteins to the Golgi, these results indicate a specific requirement for the Osh proteins in the transport of ceramide. In addition, we provide evidence that Osh proteins play a negative role in COPII vesicle biogenesis. Together, our data suggest that ceramide transport and sphingolipid levels between the ER and Golgi are maintained by two distinct functions of Osh proteins, which negatively regulate COPII vesicle formation and positively control a later stage, presumably fusion of ceramide-enriched vesicles with Golgi compartments.Ministerio de Ciencia e Innovación BFU2011-24513Junta de Andalucía P09-CVI-450

Plant viruses and viroids in Japan

An increasing number of plant viruses and viroids have been reported from all over the world due largely to metavirogenomics approaches with technological innovation. Herein, the official changes of virus taxonomy, including the establishment of megataxonomy and amendments of the codes of virus classification and nomenclature, recently made by the International Committee on Taxonomy of Viruses were summarized. The continued efforts of the plant virology community of Japan to index all plant viruses and viroids occurring in Japan, which represent 407 viruses, including 303 virus species and 104 unclassified viruses, and 25 viroids, including 20 species and 5 unclassified viroids, as of October 2021, were also introduced. These viruses and viroids are collectively classified into 81 genera within 26 families of 3 kingdoms (Shotokuvirae, Orthornavirae, Pararnavirae) across 2 realms (Monodnaviria and Riboviria). This review also overviewed how Japan’s plant virus/viroid studies have contributed to advance virus/viroid taxonomy