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The article discusses the potential for manipulating the plant mycobiome to enhance plant resilience. It explains that there are two main methods for manipulating the mycobiome: leveraging existing fungal communities or introducing novel taxa. The article also highlights the challenges and opportunities for mycobiome management, emphasizing the need for a broad understanding of plant-fungal interactions. It discusses the importance of community assembly processes, host defense mechanisms, and the maintenance of beneficial mycobiomes. The article concludes by stating that successful mycobiome manipulation will require a combination of molecular and genetic tools, as well as an understanding of the ecology and evolution of plant-fungal interactions. [Extracted from the article]

Foliar diseases of maize are among the most important diseases of maize worldwide. This study focused on 4 major foliar diseases of maize: Goss's wilt, gray leaf spot, northern corn leaf blight, and southern corn leaf blight. QTL mapping for resistance to Goss's wilt was conducted in 4 disease resistance introgression line populations with Oh7B as the common recurrent parent and Ki3, NC262, NC304, and NC344 as recurrent donor parents. Mapping results for Goss's wilt resistance were combined with previous studies for gray leaf spot, northern corn leaf blight, and southern corn leaf blight resistance in the same 4 populations. We conducted (1) individual linkage mapping analysis to identify QTL specific to each disease and population; (2) Mahalanobis distance analysis to identify putative multiple disease resistance regions for each population; and 3) joint linkage mapping to identify QTL across the 4 populations for each disease. We identified 3 lines that were resistant to all 4 diseases. We mapped 13 Goss's wilt QTLs in the individual populations and an additional 6 using joint linkage mapping. All Goss's wilt QTL had small effects, confirming that resistance to Goss's wilt is highly quantitative. We report several potentially important chromosomal bins associated with multiple disease resistance including 1.02, 1.03, 3.04, 4.06, 4.08, and 9.03. Together, these findings indicate that disease QTL distribution is not random and that there are locations in the genome that confer resistance to multiple diseases. Furthermore, resistance to bacterial and fungal diseases is not entirely distinct, and we identified lines resistant to both fungi and bacteria, as well as loci that confer resistance to both bacterial and fungal diseases. [ABSTRACT FROM AUTHOR]

The common rust disease of maize is caused by the obligate biotrophic fungus Puccinia sorghi. The maize Rp1-D allele imparts resistance against the P. sorghi IN2 isolate by initiating a defense response that includes a rapid localized programmed cell death process, the hypersensitive response (HR). In this study, to identify AvrRp1-D from P. sorghi IN2, we employed the isolation of haustoria, facilitated by a biotin-streptavidin interaction, as a powerful approach. This method proves particularly advantageous in cases where the genome information for the fungal pathogen is unavailable, enhancing our ability to explore and understand the molecular interactions between maize and P. sorghi. The haustorial transcriptome generated through this technique, in combination with bioinformatic analyses such as SignalP and TMHMM, enabled the identification of 251 candidate effectors. We ultimately identified two closely related genes, AvrRp1-D.1 and AvrRp1-D.2, which triggered an Rp1-D-dependent defense response in Nicotiana benthamiana. AvrRp1-D-induced Rp1-D-dependent HR was further confirmed in maize protoplasts. We demonstrated that AvrRp1-D.1 interacts directly and specifically with the leucine-rich repeat (LRR) domain of Rp1-D through yeast two-hybrid assay. We also provide evidence that, in the absence of Rp1-D, AvrRp1-D.1 plays a role in suppressing the plant immune response. Our research provides valuable insights into the molecular interactions driving resistance against common rust in maize., Competing Interests: The authors have declared that no competing interests exist., (Copyright: This is an open access article, free of all copyright, and may be freely reproduced, distributed, transmitted, modified, built upon, or otherwise used by anyone for any lawful purpose. The work is made available under the Creative Commons CC0 public domain dedication.)

Heterosis or hybrid vigor refers to the superior phenotypes of hybrids relative to their parental inbred lines. Recently, soil microbes were identified as an environmental driver of maize heterosis. While manipulation of the soil microbial community consistently altered heterosis, the direction of the effect appeared to be dependent on the microbiome composition, environment, or both. Abiotic factors are well-known modifiers of heterosis expression, however, how the interactive effects between the soil microbial community and abiotic factors contribute to heterosis are poorly understood. To disentangle the proposed mechanisms by which microbes influence heterosis, we characterize the variation in heterosis expression when maize was grown in soil inocula derived from active maize farms or prairies. While we did not observe consistent differences in heterosis among plants grown in these inocula, our observations reaffirm that microbial effects on heterosis are likely specific to the local microbial community. The introduction of a nutrient amendment resulted in greater heterosis expression in the presence of an agricultural inoculum but not a prairie inoculum. We also observed an effect of soil inocula and nutrient treatment on the composition of bacterial and fungal communities in the root endosphere. In addition, the interaction between soil and nutrient treatment significantly affected bacterial community composition, whereas fungal community composition was only marginally affected by this interaction. These results further suggest that the soil microbial community plays a role in maize heterosis expression but that the abiotic environment is likely a larger driver.