Expression and Role of Biosynthetic, Transporter, Receptor, and Responsive Genes for Auxin Signaling during Clubroot Disease Development

Abstract

Auxins play a pivotal role in clubroot development caused by the obligate biotroph <i>Plasmodiophora brassicae.</i> In this study, we investigated the pattern of expression of 23 genes related to auxin biosynthesis, reception, and transport in Chinese cabbage (<i>Brassica rapa</i>) after inoculation with <i>P. brassicae</i>. The predicted proteins identified, based on the 23 selected auxin-related genes, were from protein kinase, receptor kinase, auxin responsive, auxin efflux carrier, transcriptional regulator, and the auxin-repressed protein family. These proteins differed in amino acids residue, molecular weights, isoelectric points, chromosomal location, and subcellular localization. Leaf and root tissues showed dynamic and organ-specific variation in expression of auxin-related genes. The <i>BrGH3.3</i> gene, involved in auxin signaling, exhibited 84.4-fold increase in expression in root tissues compared to leaf tissues as an average of all samples. This gene accounted for 4.8-, 2.6-, and 5.1-fold higher expression at 3, 14, and 28 days post inoculation (dpi) in the inoculated root tissues compared to mock-treated roots. <i>BrNIT1,</i> an auxin signaling gene, and <i>BrPIN1,</i> an auxin transporter, were remarkably induced during both cortex infection at 14 dpi and gall formation at 28 dpi. <i>BrDCK1,</i> an auxin receptor, was upregulated during cortex infection at 14 dpi. The <i>BrLAX1</i> gene, associated with root hair development, was induced at 1 dpi in infected roots, indicating its importance in primary infection. More interestingly, a significantly higher expression of <i>BrARP1</i>, an auxin-repressed gene, at both the primary and secondary phases of infection indicated a dynamic response of the host plant towards its resistance against <i>P. brassicae</i>. The results of this study improve our current understanding of the role of auxin-related genes in clubroot disease development.