Predator-Prey Interactions in Ciliated Protists

Abstract

Protists appeared relatively early in evolution, about 1.8 billion years ago, soon after the first prokaryotic organisms. During this time period, most species developed a variety of behavioral, morphological, and physiological strategies intended to improve the ability to capture prey or to avoid predation. In this scenario, a key role was played by specialized ejectable membrane-bound organelles called extrusomes, which are capable of discharging their content to the outside of the cell in response to various stimuli. The aim of this chapter is to describe the two main strategies adopted in ciliate predatorprey interactions: (a) the first is mediated by mechanical mechanisms and involves, for example, extrusomes called trichocysts and (b) the second is mediated by toxic secondary metabolites and involves different kinds of chemical extrusomes.

Preliminary Data Related to the Effect of Climacostol Produced by the Freshwater Ciliate Climacostomum virens on Human Adenovirus

“…Initially synthesized by Masaki et al (1999) [8], it was more recently obtained as a pure compound in the natural and most bioactive Z-configuration by a novel and straightforward synthesis [9] (Figure 1). Studies on climacostol have revealed biological activity on bacterial and fungal pathogens, protozoa, human and rodent cell lines, and isolated mitochondria (see [10] for a review). These findings have indicated that the toxin exerts antimicrobial, cytotoxic, pro-apoptotic and genotoxic activities, and that it also induces dysfunctional autophagy [11].…”

Natural Function and Structural Modification of Climacostol, a Ciliate Secondary Metabolite

“…After other attacks by the same individual, the proboscis of D. margaritifer appears shorter and visibly damaged, whereas subsequent attacks can lead to the death of the predator due to the cytotoxic effect of climacostol [17]. More recently, the toxic action of climacostol against metazoan predators was also demonstrated [23], and it was furthermore assumed that C. virens is able to use climacostol for chemical offense, to paralyze and kill prey [3].…”

“…Erythrolactones: E-1 (R 1 =SO 3 ; R 2 = C 6 H 13 ); E-2 (R 1 =SO 3 ; R 2 = C 7 H 15 ); E-3 (R 1 =SO 3 ; R 2 = C 8 H 17 ); E-4 (R 1 =H; R 2 = C 6 H 13 ); E-5 (R 1 =H; R 2 = C 7 H 15 ); E-6 (R 1 =H; R 2 = C 8 H 17 ). Redrafted from [3] and reproduced under the Creative Commons attribution 3.0 license: https://creativecommons.org/licenses/by/3.0/. Climacostol (5-[(2Z)-non-2-en-1-yl]benzene-1,3-diol) is a toxic secondary metabolite physiologically produced by the freshwater ciliate Climacostomum virens ( Figure 2) for chemical defense against unicellular and multicellular predators, or for chemical offence to assist its carnivorous feeding [3,17].…”

“…Redrafted from [3] and reproduced under the Creative Commons attribution 3.0 license: https://creativecommons.org/licenses/by/3.0/. Climacostol (5-[(2Z)-non-2-en-1-yl]benzene-1,3-diol) is a toxic secondary metabolite physiologically produced by the freshwater ciliate Climacostomum virens ( Figure 2) for chemical defense against unicellular and multicellular predators, or for chemical offence to assist its carnivorous feeding [3,17]. This molecule is formed by a phenolic skeleton and a long unsaturated aliphatic hydrocarbon chain attached to the ring structure, and belongs to resorcinolic lipids (or alkenylresorcinols), a group of natural amphiphilic compounds detected in both prokaryotes and eukaryotes.…”

“…Redrafted from [3] and reproduced under the Creative Commons attribution 3.0 license: https://creativecommons.org/licenses/by/3.0/.…”