Molecular mechanism involved in the regulation of mouth-form dimorphism in nematode Pristionchus pacificus

Abstract

The ability of an organism to produce different phenotypes in response to environmental signals has been described as phenotypic plasticity. Plastic traits are ubiquitous in nature, and can have adaptive advantages as the increased variability in phenotypes provide more raw material for natural selection to act upon. In addition, plasticity can get genetically accommodated, and has been proposed to result in the origin of novel traits, and speciation. Polyphenisms are extreme forms of discrete plasticity that can be controlled by developmental switches. The dimorphism in mouth morphology of the nematode Pristionchus pacificus has been studied to decipher the mechanistic control of plasticity. This nematode can either form a narrow stenostomatous (St) mouth or a wide eurystomatous (Eu) mouth. Many environmental, genetic and epigenetic factors have been characterized to influence the decision to form one of two alternative phenotypes. The developmental switch mechanism controlling mouth-form plasticity involves a sulfatase EUD-1, and a nuclear hormone receptor NHR-40. Moreover, the polyphenism in the mouth morphology of P. pacificus is maternally influenced, and exhibits both condition dependent and stochastic regulation. The research described in this dissertation furthers the current mechanistic understanding of the mouth-form polyphenism in two major areas. First, characterization of a genetic locus that regulates the maternal influence, and exhibits a complex transcriptional activity, is performed. The alternatively spliced antisense long non-coding RNAs transcribed from this locus are also proposed to be involved in the stochastic regulation of plasticity. Second, the role of two independent sulfation processes in the regulation of mouth-form dimorphism is described. I identified a sulfotransferase that acts downstream, and independent of the previously characterized sulfatase EUD-1 to influence the mouth-form decision. This establishes the differential sulfation of biomolecules as a mechanism that can control expression of the phenotypically plastic traits.