Clubroot, caused by the obligate biotrophic protist Plasmodiophora brassicae is a devastating disease of crucifers that causes substantial economic loss worldwide. The disease is characterized by the formation of galls in the root and hypocotyl of infected plants which restricts host vascular cambium development inhibiting efficient water and nutrient uptake by the plant. The pathogen-driven interference of hormonal homeostasis, particularly of cytokinin, in the root tissue is intricately linked with induction of hypertrophy and cell divisions leading to formation of galls. Levels of cytokinins and cell division generally increase at the onset of the disease which declines at the later stages of gall formation. The genes involved cytokinin biosynthesis such as cytokinin oxidase/dehydrogenases and isopentenyl transferases shows differential expressions during clubroot infection and gall expansion in root tissues. Wider understanding of the roles of cytokinins and associated genes along the development of the disease will be helpful in unravelling plants defense mechanism against clubroot disease.

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Molecular genetic studies of self-incompatibility (SI) are the most accentuating part in the way of advancement of reproductive mechanisms in flowering plants. In the Brassicaceae plants, self-incompatibility has been mapped genetically to a single chromosomal location where several closely linked genes have been identified. Recently, various studies have provided a novel insight into the basis of specificity in the S-receptor kinase (SRK) and S-locus protein 11 or S-locus Cysteine-rich (SP11/SCR) interaction, the nature of the signaling cascade that culminates in the inhibition of ‘self’ pollen, and the physiological and morphological changes that are associated with transitions between the outbreeding and inbreeding modes of mating in the Brassicaceae. In this review, we discuss the current view of the molecular genetic aspects of the self-incompatibility in Brassicaceae.

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