Plants are exposed to a variety of devastating pathogens, causing significant yearly yield losses. In order to facilitate infections, plant pathogens secrete an arsenal of molecules termed effectors, which are known to modulate plant immune responses. Plants, on the other hand, possess receptors allowing them to detect invading pathogens by either recognising conserved molecules associated with invading microbes or by perceiving effector molecules. For decades, molecular phytopathology research has been focused on the bilateral molecular crosstalk between plants and pathogens and has deepened our understanding of virulence and defence mechanisms. In recent years, the impact of the plant microbiome on plant-pathogen interactions has gained interest, given the fact that some microbes can aid protection against invading pathogens, and pathogen invasion substantially modulates microbiome composition. Several antimicrobial effectors have been identified in fungal plant pathogens, pointing to direct mechanisms whereby pathogens can alter their hosts' microbiome to promote host colonisation. These new findings highlight that some effectors may have several functions targeting plant processes and fungi or bacteria associated with the plant. Advances in computational biology have greatly enhanced the analysis of predicted effector proteins and revealed that these often are highly conserved among phylogenetically distant fungi. Comparative analyses of protein structures have also revealed that functional divergence may emerge from changes in surface frustration around conserved protein folds. Further, computational simulations of protein evolution indicate that protein properties associated with (antimicrobial) effectors can emerge rapidly around conserved folds. We here summarise and discuss recent studies based on computational biology methods, providing novel insights into effector origin, evolution, and functional divergence.

The first and arguably most critical level of gene expression is transcription of the genetic information from DNA into RNA. Within this process, transcription initiation stands out as the key step that influences all downstream events. Central to initiation are promoters, DNA sequences that interact with the key enzyme of transcription, RNA polymerase. A single transcription unit may be controlled by one or multiple promoters, a strategy found across all domains of life. This review highlights how combinatorial promoter arrangements control gene expression in microorganisms, with brief comparisons to other organisms. We also explore how these promoter architectures function as sensors for stress-related molecules, such as antibiotics. We examine how these insights can be applied to predict previously unidentified mechanisms of antibiotic resistance. Finally, the use of dual-promoters in synthetic biology is outlined and discussed.

Phenotypic heterogeneity within isogenic bacterial populations represents a fundamental adaptation strategy that enables pathogen survival across the selective pressures of host infection. Rather than uniformly responding to environmental challenges, bacterial populations diversify through mechanisms including phase variation, stochastic gene expression, asymmetric cell division, and intercellular communication, generating functionally specialized subpopulations that operate through bet-hedging and division of labor frameworks. This review synthesizes recent advances showing how host-derived signals tune bacterial switching dynamics and deterministically partition populations into discrete phenotypic states. These functionally specialized subpopulations have clinical implications, with antibiotic-tolerant persisters representing one example of how phenotypic heterogeneity drives treatment failure and enables infection recurrence, underscoring the need to understand and target this fundamental aspect of bacterial pathogenesis.