Search

The microbial composition of the rhizosphere soil could be an important determinant of crop yield, pathogen resistance, and other beneficial attributes in plants. However, little is known about the impact of cropping sequences on microbial community dynamics, especially in economically important species like soybean. Using 2-year crop sequences of corn-soybean, canola-soybean, and soybean-soybean, we investigated how crops from the previous growing season influenced the structure of the microbiome in both the bulk soil and soybean rhizosphere. A combination of marker-based Illumina sequencing and bioinformatics analyses was used to show that bacterial species richness and evenness in the soybean rhizosphere soil were similar following canola and soybean compared to a previous corn sequence. However, fungal species richness and evenness remained unaffected by crop sequence. In addition, bacterial and fungal species diversity in both the bulk and soybean rhizosphere soil were not influenced by crop sequence. Lastly, the corn-soybean sequence significantly differed in the relative abundance of certain bacterial and fungal classes in both the soybean rhizosphere and bulk soil. While canola-soybean and a continuous soybean sequence did not, suggesting that a preceding corn sequence may reduce the occurrence of overall bacterial and fungal community members. For the present study, crop sequence impacts bacterial diversity and richness in both the bulk soil and soybean rhizosphere soil whereas fungal diversity and richness are resilient to crop sequence practices. Together, these findings could help drive decision making for annual crop and soil management practices. [ABSTRACT FROM AUTHOR]

In vitro inhibition of the fungal pathogen Sclerotinia sclerotiorum by Pseudomonas chlororaphis PA23 is reliant upon a LysR-type transcriptional regulator (LTTR) called PtrA. In the current study, we show that Sclerotinia stem rot and leaf infection are significantly increased in canola plants inoculated with the ptrA-mutant compared to the wild type, establishing PtrA as an essential regulator of PA23 biocontrol. LTTRs typically regulate targets that are upstream of and divergently transcribed from the LTTR locus. We identified a short chain dehydrogenase (scd) gene immediately upstream of ptrA. Characterization of a scd mutant revealed that it is phenotypically identical to the wild type. Moreover, scd transcript abundance was unchanged in the ptrA mutant. These findings indicate that PtrA regulation does not involve scd, rather this LTTR controls genes located elsewhere on the chromosome. Employing a combination of complementation and transcriptional analysis we investigated whether connections exist between PtrA and other regulators of biocontrol. Besides ptrA, gacS was the only gene able to partially rescue the wild-type phenotype, establishing a connection between PtrA and the sensor kinase GacS. Transcriptomic analysis revealed decreased expression of biosynthetic (phzA, prnA) and regulatory genes (phzI, phzR, rpoS, gacA, rsmX, rsmZ, retS) in the ptrA mutant; conversely, rsmE, and rsmY were markedly upregulated. The transcript abundance of ptrA was nine-fold higher in the mutant background indicating that this LTTR negatively autoregulates itself. In summary, PtrA is an essential regulator of genes required for PA23 biocontrol that is functionally intertwined with GacS. [ABSTRACT FROM AUTHOR]

Pathogenic fungi have diverse growth lifestyles that support fungal colonization on plants. Successful colonization and infection for all lifestyles depends upon the ability to modify living host plants to sequester the necessary nutrients required for growth and reproduction. Secretion of virulence determinants referred to as "effectors" is assumed to be the key governing factor that determines host infection and colonization. Effector proteins are capable of suppressing plant defense responses and alter plant physiology to accommodate fungal invaders. This review focuses on effector molecules of biotrophic and hemibiotrophic plant pathogenic fungi, and the mechanism required for the release and uptake of effector molecules by the fungi and plant cells, respectively. We also place emphasis on the discovery of effectors, difficulties associated with predicting the effector repertoire, and fungal genomic features that have helped promote effector diversity leading to fungal evolution. We discuss the role of specific effectors found in biotrophic and hemibiotrophic fungi and examine how CRISPR/Cas9 technology may provide a new avenue for accelerating our ability in the discovery of fungal effector function. [ABSTRACT FROM AUTHOR]