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As zinc finger protein transcription factors (TFs), the molecular mechanism of Cys-Cys-Cys-His (CCCH) TFs in regulating plant development, growth and stress response has been well studied. However, the roles of CCCH TFs in fruit ripening are still obscure. Herein, we report that MaCCCH33-like2 TF and its associated proteins modulate the fruit softening of 'Fenjiao' bananas. MaCCCH33-like2 interacts directly with the promoters of three genes: isoamylase2 (MaISA2), sugar transporter14-like (MaSUR14-like) and β- d -xylosidase23 (MaXYL23), all of which are responsible for encoding proteins involved in the degradation of starch and cell wall components. Additionally, MaCCCH33-like2 forms interactions with abscisic acid–insensitive 5 (ABI5)-like and ethylene F-box protein 1 (MaEBF1), resulting in enhanced binding and activation of promoters of genes related to starch and cell wall degradation. When MaCCCH33-like2 is transiently and ectopically overexpressed in 'Fenjiao' banana and tomato fruit, it facilitates softening and ripening processes by promoting the degradation of cell wall components and starch and the production of ethylene. Conversely, the temporary silencing of MaCCCH33-like2 using virus-induced gene silencing (VIGS) inhibits softening and ripening in the 'Fenjiao' banana by suppressing ethylene synthesis, as well as starch and cell wall degradation. Furthermore, the promoter activity of MaCCCH33-like2 is regulated by MaABI5-like. Taken together, we have uncovered a novel MaCCCH33-like2/MaEBF1/MaABI5-like module that participates in fruit softening regulation in bananas. [ABSTRACT FROM AUTHOR]

Banana is a typical subtropical fruit, sensitive to chilling injuries and prone to softening disorder. However, the underlying regulatory mechanisms of the softening disorder caused by cold stress remain obscure. Herein, we found that BEL1‐LIKE HOMEODOMAIN transcription factor 1 (MaBEL1) and its associated proteins regulate the fruit softening and ripening process. The transcript and protein levels of MaBEL1 were up‐regulated with fruit ripening but severely repressed by the chilling stress. Moreover, the MaBEL1 protein interacted directly with the promoters of the cell wall and starch degradation‐related genes, such as MaAMY3, MaXYL32, and MaEXP‐A8. The transient overexpression of MaBEL1 alleviated fruit chilling injury and ripening disorder caused by cold stress and promoted fruit softening and ripening of "Fenjiao" banana by inducing ethylene production and starch and cell wall degradation. The accelerated ripening was also validated by the ectopic overexpression in tomatoes. Conversely, MaBEL1‐silencing aggravated the chilling injury and ripening disorder and repressed fruit softening and ripening by inhibiting ethylene production and starch and cell wall degradation. MaABI5‐like and MaEBF1, the two positive regulators of the fruit softening process, interacted with MaBEL1 to enhance the promoter activity of the starch and cell wall degradation‐related genes. Moreover, the F‐box protein MaEBF1 does not modulate the degradation of MaBEL1, which regulates the transcription of MaABI5‐like protein. Overall, we report a novel MaBEL1‐MaEBF1‐MaABI5‐like complex system that mediates the fruit softening and ripening disorder in "Fenjiao" bananas caused by cold stress. [ABSTRACT FROM AUTHOR]

The accuracy of flatness actuator efficiency (FAE) is a prerequisite to achieve high precision automatic flatness control. This study proposes an accurate acquisition approach of FAE based on the combination of simulation modeling and data‐driven modeling for flatness control of cold‐rolled strip. First, a 3D rolling feature space model is constructed according to the change interval of rolling process parameters based on rolling conditions. A 3D finite element simulation model is subsequently established to determine the prior value of actuator efficiency at each node in the feature space model. Then, to improve the accuracy of prior value, an online optimization model is developed by means of data‐driven mechanism. The sorting algorithm and the central limit theorem are introduced to filter the measured process data and calculate the variable weighting. The processed data are imported into the model to improve the fitting model. Finally, a linear output prediction model based on the trend extrapolation method is proposed to realize the accurate acquisition of FAE under any rolling conditions. The data analysis of the production process shows that the model is adaptive and accurate, which can realize high precision flatness control. [ABSTRACT FROM AUTHOR]

This paper presents a general model based on time Petri net, capable of handling both qualitative and quantitative temporal information. Both metric relations between time points and qualitative relations between time interval can be encoded in a model. This model also allows the representation of higher-order expression and repeated activities which constitute a large part of the normal schedule. In addition, graphical representation of a time Petri net gives a straightforward view of relations between temporal objects.

Coronavirus disease 2019 (COVID‐19) is a global pandemic caused by severe acute respiratory syndrome coronavirus 2 (SARS‐CoV‐2). The models that can accurately resemble human‐relevant responses to viral infection are lacking. Here, a biomimetic human disease model on chip that allows to recapitulate lung injury and immune responses induced by SARS‐CoV‐2 in vitro at organ level is created. This human alveolar chip reproduce the key features of alveolar‐capillary barrier by coculture of human alveolar epithelium, microvascular endothelium, and circulating immune cells under fluidic flow in normal and disease. Upon SARS‐CoV‐2 infection, the epithelium exhibits higher susceptibility to virus than endothelium. Transcriptional analyses show activated innate immune responses in epithelium and cytokine‐dependent pathways in endothelium at day 3 post‐infection, revealing the distinctive responses in different cell types. Notably, viral infection causes the immune cell recruitment, endothelium detachment, and increased inflammatory cytokines release, suggesting the crucial role of immune cells involved in alveolar barrier injury and exacerbated inflammation. Treatment with remdesivir can inhibit viral replication and alleviate barrier disruption on chip. This organ chip model can closely mirror human‐relevant responses to SARS‐CoV‐2 infection, which is difficult to be achieved by in vitro models, providing a unique platform for COVID‐19 research and drug development. [ABSTRACT FROM AUTHOR]