Changbo Dai

Aluminium (Al) toxicity severely limits crop productivity in acidic soils by inhibiting root growth and nutrient uptake, yet the hormonal mechanisms coordinating Al defence in tobacco remain unclear. Here, we show that Al stress rapidly induces gibberellin (GA) biosynthesis in tobacco roots, and that GA signalling mitigates Al toxicity by promoting root growth and reducing Al accumulation. Using exogenous GA application, CRISPR/Cas9‐mediated NtGA3‐ox1 mutants, GA biosynthesis inhibitors, transcriptomic profiling, and biochemical analyses, we demonstrate that GA enhances Al exclusion through two complementary mechanisms: remodelling root cell wall composition, particularly by increasing hemicellulose content to sequester Al, and reinforcing the endodermal Casparian strip (CS) through the upregulation of CS‐associated genes. Pharmacological manipulation of lignin biosynthesis confirms that early CS formation was critical for restricting Al entry. These findings reveal GA as a dynamic regulator of Al stress adaptation, coordinating structural and biochemical defences to maintain root growth, and highlight GA signalling as a potential target for improving crop tolerance to Al‐toxic acidic soils.

In recent years, CRISPR/Cas gene editing technology has become a fundamental method in biological breeding. As a vital tool for overcoming technological obstacles, it is currently widely used in functional gene research and genetic enhancement across a variety of organisms. Currently, CRISPR activation (CRISPRa) technology based on dCas9 fusion transcription activation domains has emerged as a powerful tool for expanding the application of CRISPR/Cas systems in improving traits in plants, animals, and microorganisms. This overview starts by going over the underlying principles and components of gene activation editing technology, as well as the phases of development of its three generations. It summarises the present difficulties and potential directions in this field while concentrating on the use of gene activation editing in important crop traits including growth and development regulation, stress resistance, and quality regulation. The objective is to offer valuable insights for the research and development of crop breeding.

The release and outgrowth of axillary buds are essential parts of the process of shoot branching in plants, but knowledge of the underlying regulatory mechanisms remains limited. Analysis of mab1‐D , a tobacco mutant with a greater number of axillary branches, showed that the mutant phenotype resulted from positive modulation of axillary buds release and outgrowth. TAIL‐PCR and co‐separation analyses suggested that NtMAB1‐S1 , a member of the Related to ABI3/VP1 ( RAV ) subfamily that was highly expressed in the base of axillary buds, was associated with the mutant phenotype. Phenotypic analyses of mab1‐D overexpression, knockdown, knockout and complementation lines demonstrated that NtMAB1‐S1 was a positive regulator of axillary buds release and outgrowth. NtMAB1‐S1 accelerated these processes through transcriptional repression via the B3 repression domain. RNA‐sequencing analysis revealed that NtMAB1‐S1 was involved in the trehalose‐6‐phosphate and gibberellin metabolism pathways. Moreover, NtMAB1‐S1 enhanced the release and outgrowth of axillary buds by directly repressing transcription of NtTPPF , a trehalose‐6‐phosphate phosphatase, and NtGA2ox8 , a gibberellin oxidase. NtMAB1‐S1 thus plays a pivotal role in regulating the release and outgrowth of axillary buds and is a potential target for genetic interventions aimed at shaping ideal plant architecture.

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Glyphosate is a widely used non-selective, broad-spectrum, systemic herbicide by interfering with the biosynthesis of aromatic amino acids. However, the emergence of glyphosate-resistant weeds has driven the need for enhanced herbicide resistance in crops. In this study, we engineered two mutant variants of the tobacco EPSPS gene through amino acid substitution (TIPS-NtEPSPS and P180S-NtEPSPS). These mutated EPSPS genes were overexpressed in tobacco under the control of CaMV35S promoters. Our results demonstrate that overexpression of TIPS-NtEPSPS significantly enhances glyphosate tolerance, allowing plants to withstand up to four times the recommended dose without compromising their fitness. This research highlights the potential of the TIPS-NtEPSPS mutant to improve herbicide resistance in tobacco, offering a viable approach for effective weed management.

Dichloroquinolinic acid is a hormone-type herbicide widely used to control barnyard grass during crop cultivation. However, it can seriously inhibit the growth of susceptible crops, including tobacco, because it degrades slowly under field conditions. Additionally, the mechanism by which it damages crops is unclear. More specifically, the transcriptional changes in plants induced by dichloroquinolinic acid remain unknown. In this study, differentially expressed genes (DEGs) in tobacco treated with dichloroquinolinic acid (varying concentrations and durations) were analyzed and validated to explore the global transcriptome changes. The number of DEGs, which were determined according to the FPKM, varied from 758 to 21,340. The KEGG analysis revealed that many DEGs were involved in starch and sucrose metabolism, phenylpropanoid biosynthesis, photosynthesis, porphyrin and chlorophyll metabolism, and glutathione metabolism. Transcriptomic analyses indicated that dichloroquinolinic acid can inhibit tobacco growth by inhibiting photosynthesis and storage of energy. We discovered that the toxicity mechanism of the hormone herbicide dichloroquinolinic acid differs from that of high concentrations of IAA (Indoleacetic acid), despite studies confirming that the effects of hormone herbicides are consistent with the physiological disturbances and growth inhibition exhibited by plants in IAA overdose. Particularly, dichloroquinolinic acid suppresses photosynthesis while high concentration IAA stimulates nucleotide synthesis and photosynthesis. More importantly, we found by editing the IAA-responsive gene IAA16, tobacco could develop resistance to dichloroquinolinic acid. The results will help clarify plant responses to hormone-type herbicides at the transcriptional level, thereby providing insights into the diversity in the gene’s response to herbicides, the molecular targets of hormone-type herbicides, and the mechanism underlying the susceptibility of tobacco to dichloroquinolinic acid. Accordingly, this study may be helpful for future research to enhance crop resistance to herbicides residues.