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Lipopeptides, a class of compounds consisting of a peptide ring and a fatty acid chain, are secondary metabolites produced by Bacillus spp. As their hydrophilic and oleophilic properties, lipopeptides are widely used in food, medicine, environment and other industrial or agricultural fields. Compared with artificial synthetic surfactants, microbial lipopeptides have the advantages of low toxicity, high efficiency and versatility, resulting in urgent market demand and broad development prospect of lipopeptides. However, due to the complex metabolic network and precursor requirements of synthesis, the specific and strict synthesis pathway, and the coexistence of multiple homologous substances, the production of lipopeptides by microorganisms has the problems of high cost and low production efficiency, limiting the mass production of lipopeptides and large-scale application in industry. This review summarizes the types of Bacillus-produced lipopeptides and their biosynthetic pathways, introduces the versatility of lipopeptides, and describes the methods to improve the production of lipopeptides, including genetic engineering and optimization of fermentation conditions. [ABSTRACT FROM AUTHOR]

SUMMARY: Chilling stress causes banana fruit softening disorder and severely impairs fruit quality. Various factors, such as transcription factors, regulate fruit softening. Herein, we identified a novel regulator, MaC2H2‐IDD, whose expression is closely associated with fruit ripening and softening disorder. MaC2H2‐IDD is a transcriptional activator located in the nucleus. The transient and ectopic overexpression of MaC2H2‐IDD promoted "Fenjiao" banana and tomato fruit ripening. However, transient silencing of MaC2H2‐IDD repressed "Fenjiao" banana fruit ripening. MaC2H2‐IDD modulates fruit softening by activating the promoter activity of starch (MaBAM3, MaBAM6, MaBAM8, MaAMY3, and MaISA2) and cell wall (MaEXP‐A2, MaEXP‐A8, MaSUR14‐like, and MaGLU22‐like) degradation genes. DLR, Y1H, EMSA, and ChIP‐qPCR assays validated the expression regulation. MaC2H2‐IDD interacts with MaEBF1, enhancing the regulation of MaC2H2‐IDD to MaAMY3, MaEXP‐A2, and MaGLU22‐like. Overexpressing/silencing MaC2H2‐IDD in banana and tomato fruit altered the transcript levels of the cell wall and starch (CWS) degradation genes. Several differentially expressed genes (DEGs) were authenticated between the overexpression and control fruit. The DEGs mainly enriched biosynthesis of secondary metabolism, amino sugar and nucleotide sugar metabolism, fructose and mannose metabolism, starch and sucrose metabolism, and plant hormones signal transduction. Overexpressing MaC2H2‐IDD also upregulated protein levels of MaEBF1. MaEBF1 does not ubiquitinate or degrade MaC2H2‐IDD. These data indicate that MaC2H2‐IDD is a new regulator of CWS degradation in "Fenjiao" banana and cooperates with MaEBF1 to modulate fruit softening, which also involves the cold softening disorder. Significance Statement: MaC2H2‐IDD/MaEBF1 complex modulates banana fruit softening by regulating genes related to starch and cell wall degradation. Chilling stress severely represses the activation of softening‐related genes, causing fruit ripening disorder and impairing the texture quality. [ABSTRACT FROM AUTHOR]

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]

Low-temperature storage is a common strategy for preserving and transporting vegetables and fruits. However, many fruits are hypersensitive to chilling injury, including bananas. In the present study, storage conditions of 11 °C delayed the ripening of Fenjiao (Musa ABB Pisang Awak) banana, and the pulp could be softened after ethephon treatment. Storage conditions of 7 °C prevented fruit from fully softening, and fruit contained a significantly higher starch content and lower soluble sugar content. MaEBF1, a critical gene component in the ethylene signaling pathway, was repressed during ripening after fruit had been stored for 12 days at 7 °C. The expression of a series of starch degradation-related genes and a MaNAC67-like gene were also severely repressed. Both MaEBF1 and MaNAC67-like genes were ethylene-inducible and localized in the nucleus. MaNAC67-like protein was able to physically bind to the promoter of genes associated with starch degradation, including MaBAM6, MaSEX4, and MaMEX1. Yeast two-hybrid, GST-pull down, and BiFC assays showed that MaEBF1 interacted with the MaNAC67-like protein, and their interaction further activated the promoters of MaBAM6 and MaSEX4. The current study indicates that MaNAC67-like is a direct regulator of starch degradation and potential for involvement in regulating chilling-inhibited starch degradation by interacting with the ethylene signaling components in banana fruit. The present work paves the way for further functional analysis of MaEBF1 and MaNAC67-like in banana, which will be useful for understanding the regulation of banana starch metabolism and fruit ripening. [ABSTRACT FROM AUTHOR]

Cold stress adversely affects plant production, both qualitatively and quantitatively. Banana (Musa acuminata) is sensitive to cold stress and suffers chilling injury (CI) when stored under 11°C, causing abnormal fruit softening. However, the mechanism underlying the abnormal fruit softening due to CI remains obscure. This study uncovered the coordinated transcriptional mechanism of ethylene F-box (EBF1) protein and abscisic acid-insensitive 5 (ABI5)-like protein in regulating chilling-induced softening disorders of Fenjiao banana. Cold stress severely inhibited the transcript and protein levels of EBF1, ABI5-like, and fruit softening-related genes. The ABI5-like protein bound to the promoters of key starch and cell wall degradation-related genes such as β-amylase 8 (BAM8), pectate lyase 8 (PL8), and β-D-xylosidase23-like (XYL23-like) and activated their activities. EBF1 physically interacted with ABI5-like and enhanced the transcriptional activity of the key starch and cell wall degradation-related genes but did not ubiquitinate or degrade ABI5-like protein. This promoted fruit ripening and ameliorated fruit CI in a manner similar to the effect of exogenous abscisic acid treatment. The ectopic and transient overexpression of EBF1 and ABI5-like genes in tomato (Solanum lycopersicum) and Fenjiao banana accelerated fruit ripening and softening by promoting ethylene production, starch and cell wall degradation, and decreasing fruit firmness. EBF1 interacted with EIL4 but did not ubiquitinate or degrade EIL4, which is inconsistent with the typical role of EBF1/2 in Arabidopsis (Arabidopsis thaliana). These results collectively highlight that the interaction of EBF1 and ABI5-like controls starch and cell wall metabolism in banana, which is strongly inhibited by chilling stress, leading to fruit softening and ripening disorder., (© American Society of Plant Biologists 2021. All rights reserved. For permissions, please email: journals.permissions@oup.com.)