Cell walls are basically complex with dynamic structures that are being involved in several growth and developmental processes, as well as responses to environmental stresses and the defense mechanism. Pectin is secreted into the cell wall in a highly methylesterified form. It is able to perform function after the de-methylesterification by pectin methylesterase (PME). Whereas, the pectin methylesterase inhibitor (PMEI) plays a key role in plant cell wall modification through inhibiting the PME activity. It provides pectin with different levels of degree of methylesterification to affect the cell wall structures and properties. The PME activity was analyzed in six tissues of Sorghum bicolor, and found a high level in the leaf and leaf sheath. PMEI families have been identified in many plant species. Here, a total of 55 pectin methylesterase inhibitor genes (PMEIs) were identified from S. bicolor whole genome, a more detailed annotation of this crop plant as compared to the previous study. Chromosomal localization, gene structures and sequence characterization of the PMEI family were analyzed. Moreover, cis-acting elements analysis revealed that each PMEI gene was regulated by both internal and environmental factors. The expression patterns of each PMEI gene were also clustered according to expression pattern analyzed in 47 tissues under different developmental stages. Furthermore, some SbPMEIs were induced when treated with hormonal and abiotic stress. Taken together, these results laid a strong foundation for further study of the functions of SbPMEIs and pectin modification during plant growth and stress responses of cereal.

Pectin methylesterases (PMEs) are key enzymes that regulate the structure and function of pectin in plant cell walls. By fine-tuning the degree and pattern

The Arabidopsis ( Arabidopsis thaliana ) seed coat mucilage is a specialized cell wall with pectin as its major component. Pectin is synthesized in the Golgi apparatus with homogalacturonan fully methylesterified, but it must undergo de-methylesterification by pectin methylesterase (PME) after being secreted into the cell wall. This reaction is critical for pectin maturation, but the mechanisms of its transcriptional regulation remain largely unknown. Here, we show that the Arabidopsis ERF4 transcription factor positively regulates pectin de-methylesterification during seed development and directly suppresses the expression of PME INHIBITOR13 ( PMEI13 ), 14 , 15 and SUBTILISIN-LIKE SERINE PROTEASE 1.7 ( SBT1.7 ). The erf4 mutant seeds showed repartitioning of mucilage between soluble and adherent layers as a result of decreased PME activity and increased degree of pectin methylesterification. ERF4 physically associates with and antagonizes MYB52 in activating PMEI6 , 14 and SBT1.7 and MYB52 also antagonizes ERF4 activity in the regulation of downstream targets. Gene expression studies revealed that ERF4 and MYB52 have opposite effects on pectin de-methylesterification. Genetic analysis indicated that the erf4-2 myb52 double mutant seeds show mucilage phenotype similar to wild-type. Taken together, this study demonstrates that ERF4 and MYB52 antagonize each other’s activity to maintain the appropriate degree of pectin methylesterification, expanding our understanding of how pectin de-methylesterification is fine-tuned by the ERF4-MYB52 transcriptional complex in the seed mucilage. One-sentence summary: Arabidopsis ERF4 and MYB52 transcription factors interact and play antagonistic roles in regulating homogalacturonan de-methylesterification related genes in the seed coat mucilage.

Bacterial wilt is a devastating vascular disease caused by the soil-borne bacterium Ralstonia solanacearum , which invades and blocks the xylem of susceptible plants, especially economically important solanaceous crops. In addition to classical plant defense hormones, recent research has focused on understanding the role of auxin as a key and continuous regulator of infection and development. Auxin connects changes during infection to root development and the progression of bacterial wilt disease. The auxin related shift in plant hormone patterns associated with root development has been observed in both infected and non-infected host plant species. This shift is accompanied by the upregulation of several auxin regulating transcriptional programs, the accumulation of indole-3-acetic acid, and the enhancement of auxin signaling in specific plant tissues. The auxin-associated reprogramming of roots infected with R. solanacearum is also linked to the reorganization of root developmental programs, including reduced primary root elongation, pronounced induction of root hair formation, and increased lateral root development at later stages of infection. Root hair formation in response to infection requires an intact and functional auxin signaling pathway. There is also support for a positive relationship between the level of auxin responsiveness and a plant’s susceptibility to infection. Susceptible genotypes activate their auxin pathway more than resistant genotypes, while reducing the ability to transport or perceive auxin increases plant resistance and decreases the severity of key root-associated phenotypes during infections. At the molecular level, R. solanacearum is reported to influence the auxin homeostasis of the host plant indirectly through effectors, which induce changes in the plant immune response, alter metabolism and energy status, and modify the interactions within plant hormone pathways. These changes create conditions that facilitate the colonization and spread of R. solanacearum . Therefore, auxin is best understood as a dynamically regulated “balancer” that mediates the trade-off between plant growth and defense, integrating the plant developmental flexibility with immune response. Furthermore, leveraging these findings to develop precision resistance offers strategies for enhancing plant resistance. These include improving auxin modulation within the growth environment and employing spatiotemporal transcriptomics to identify spatially and temporally correlated losses of auxin sensitivity or transport in root zones susceptible to infection.

In plants, the beta galactosidases (BGALs) function in various biological processes, including growth, development and responses to abiotic stresses. Howev