During the past several decades, numerous reports from disparate geographical areas have documented an increased frequency of "bleaching" in reef-forming corals. The phenomenon, triggered by increased sea surface temperatures, occurs when the cnidarian hosts digest and/or expel their intracellular, photosynthetic dinoflagellate symbionts ("zooxanthellae" in the genus Symbiodinium). Although coral bleaching is often followed by the death of the animal hosts, in some cases, the animal survives and can be repopulated with viable zooxanthellae. The physiological factors determining the ability of the coral to survive bleaching events are poorly understood. In this study, we experimentally established that bleaching and death of the host animal involve a caspase-mediated apoptotic cascade induced by reactive oxygen species produced primarily by the algal symbionts. In addition, we demonstrate that, although some corals naturally suppress caspase activity and significantly reduce caspase concentration under high temperatures as a mechanism to prevent colony death from apoptosis, even sensitive corals can be prevented from dying by application of exogenous inhibitors of caspases. Our results indicate that variability in response to thermal stress in corals is determined by a four-element, combinatorial genetic matrix intrinsic to the specific symbiotic association. Based on our experimental data, we present a working model in which the phenotypic expression of this symbiont/host relationship places a selective pressure on the symbiotic association. The model predicts the survival of the host animals in which the caspase-mediated apoptotic cascade is down-regulated.

Certain stony corals can alternate between a calcifying colonial form and noncalcifying solitary polyps, supporting the hypothesis that corals have survived through geologic timescale periods of unfavorable calcification conditions. However, the mechanisms enabling this biological plasticity are yet to be identified. Here we show that incubation of two coral species (Pocillopora damicornis and Oculina patagonica) under reduced pH conditions (pH 7.2) simulating past ocean acidification induce tissue-specific apoptosis that leads to the dissociation of polyps from coenosarcs. This in turn leads to the breakdown of the coenosarc and, as a consequence, to loss of coloniality. Our data show that apoptosis is initiated in the polyps and that once dissociation between polyp and coenosarc terminates, apoptosis subsides. After reexposure of the resulting solitary polyps to normal pH (pH 8.2), both coral species regenerated coenosarc tissues and resumed calcification. These results indicate that regulation of coloniality is under the control of the polyp, the basic modular unit of the colony. A mechanistic explanation for several key evolutionarily important phenomena that occurred throughout coral evolution is proposed, including mechanisms that permitted species to survive the third tier of mass extinctions.apoptosis | ocean acidification | corals

Elevated seawater temperatures are associated with coral bleaching events and related mortality. Nevertheless, some coral species are able to survive bleaching and recover. The apoptotic responses associated to this ability were studied over 3 years in the coral Stylophora pistillata from the Gulf of Eilat subjected to long term thermal stress. These include caspase activity and the expression profiles of the S. pistillata caspase and Bcl-2 genes (StyCasp and StyBcl-2-like) cloned in this study. In corals exposed to thermal stress (32 or 34°C), caspase activity and the expression levels of the StyBcl-2-like gene increased over time (6–48 h) and declined to basal levels within 72 h of thermal stress. Distinct transcript levels were obtained for the StyCasp gene, with stimulated expression from 6 to 48 h of 34°C thermal stress, coinciding with the onset of bleaching. Increased cell death was detected in situ only between 6 to 48 h of stress and was limited to the gastroderm. The bleached corals survived up to one month at 32°C, and recovered back symbionts when placed at 24°C. These results point to a two-stage response in corals that withstand thermal stress: (i) the onset of apoptosis, accompanied by rapid activation of anti-oxidant/anti-apoptotic mediators that block the progression of apoptosis to other cells and (ii) acclimatization of the coral to the chronic thermal stress alongside the completion of symbiosis breakdown. Accordingly, the coral's ability to rapidly curb apoptosis appears to be the most important trait affecting the coral's thermotolerance and survival.

Streptococcus iniae was isolated from 2 moribund wild Red Sea fishes, Pomadasys stridens (Pomadasyidae) and Synodus variegatus (Synodontidae), both collected in shallow waters along the Israeli coast of the Gulf of Eilat. The site is approximately 2 km from a mariculture cage farm in which streptococcal infections were diagnosed in previous years in the red drum Sciaenops ocellatus. This is the first report of S. iniae in Red Sea fishes. Biochemical and molecular similarities between the isolates from cultured fishes and those from the wild specimens suggest that a single strain is involved, and that 'amplification' and dispersal of this pathogen from captive to feral fishes have occurred. At the molecular level, the pathogen is different from the S. iniae isolates that have been afflicting the Israeli freshwater aquaculture in recent years. Although S. iniae prevalence in the wild fish populations of the area remains to be determined, the northernmost region of the Gulf of Eilat, virtually landlocked and with generally calm seas and weak currents, seems to be particularly vulnerable to the impact of diseases that develop in this mariculture system. KEY WORDS: Fish disease · Mariculture · Red drum · Sciaenops ocellatus · Sea bass · Dicentrarchus labrax · Tilapia · Oreochromis mossambicus · 16S rRNA · PCR Resale or republication not permitted without written consent of the publisherDis Aquat Org 49: [165][166][167][168][169][170] 2002 populations increases the opportunity for disease transmission in both directions, since translocated species may not only be extremely sensitive to a local pathogen but may themselves carry exotic diseases that can spread to indigenous wild populations (Paperna 1998).In the Eilat region, streptococcosis has recurred repeatedly since it was first diagnosed in 1996 in the red drum (see Table 1). During the summer of 2000, persistent mortalities of wild fishes in the shallow waters of Eilat's northern coast were investigated. Gram-positive cocci in chains were isolated from 2 moribund wild specimens and compared with streptococcal isolates from fishes cultured in this region in previous years. MATERIALS AND METHODS Fishes.The infection chronology, sources of isolation and list of fish hosts are summarized in Table 1. The first case was diagnosed in 1995 in a stock of European sea bass Dicentrarchus labrax submitted to our laboratory for examination from a fish farm in Ashdod, on the Mediterranean coast of Israel. All subsequent cases refer to fish grown in the Eilat area (Red Sea). Water in this region is subjected to limited seasonal fluctuations of temperature (23 ± 1.5°C) and salinity (40 ± 1 ‰). Red drum Sciaenops ocellatus were examined during mortality outbreaks in the cages. The tilapia Oreochromis mossambicus, adapted to seawater, were maintained at Israel Oceanographic and Limnological Research National Center for Mariculture in the facilities of the Reproduction Department for experimental purposes. The lined piggy Pomadasys stridens (Pomadasyidae) and the lizar...

Infection patterns of Mycobacterium rnarinum were studied over a period of 3 yr in wild rabbitfish Siganus rivulatus populations associated with commercial mariculture cages and inhabiting various sites along the Israeli Red Sea coastline. Mycobacteriosis was first recorded from the Red Sea in 1990 in farmed sea bass Dicentrarchus labrax and is absent from records of studies on parasites and diseases of wild rabbitfish carned out in the 1970s and 1980s. A sharp increase in the prevalence of the dsease in cultured and wild fish in the region has occurred since. A total of 1142 rabbitfish were examined over a 3 yr period from inside mariculture net cages, from the cage surroundings and from several sites along the coast. Histological sections of spleens were examined for presence of granulomatous lesions. Overall prevalence levels of 50 % were recorded in the rabbitfish sampled inside the net cages and 39 % at the cages' close surroundings, 21 % at a sandy beach site 1.2 km westwards, 35 % at Eilat harbour 3 km to the south and 4 2 % at a coral reef site about 10 km south of the cages. In addition, 147 fish belonging to 18 native Red Sea species were sampled from 2 sites, the net cage farm perimeter and the coral reef area, and examined for similar lesions. None of those from the coral reef were infected with Mycobacterium; however, 9 of 14 species collected from the cage surroundings were infected. An increase in prevalence of mycobacteriosis in the manculture farm area was noted from 1995 to 1997. At the same time, a significant increase in prevalence was also apparent at the coral reef sampling site. Two M. marinum isolates from rabbitfish captured at Eilat harbour and the coral reef site were shown by 16s rDNA sequencing analysis to be identical to isolates from rabbitfish trapped inside the mariculture cages as well as isolates from locally cultured sea bass D. labrax. The implications of spreading of M, marinum infection in wild fish populations in the Gulf of Eilat are discussed.

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Recent studies suggest that controlled apoptotic response provides an essential mechanism, enabling corals to respond to global warming and ocean acidification. However, the molecules involved and their functions are still unclear. To better characterize the apoptotic response in basal metazoans, we studied the expression profiles of selected genes that encode for putative pro- and anti-apoptotic mediators in the coral Stylophora pistillata under thermal stress and bleaching conditions. Upon thermal stress, as attested by the elevation of the heat-shock protein gene HSP70’s mRNA levels, the expression of all studied genes, including caspase, Bcl-2, Bax, APAF-1 and BI-1, peaked at 6–24 h of thermal stress (hts) and declined at 72 hts. Adversely, the expression levels of the survivin gene showed a shifted pattern, with elevation at 48–72 hts and a return to basal levels at 168 hts. Overall, we show the quantitative anti-apoptotic traits of the coral Bcl-2 protein, which resemble those of its mammalian counterpart. Altogether, our results highlight the similarities between apoptotic networks operating in simple metazoans and in higher animals and clearly demonstrate the activation of pro-cell survival regulators at early stages of the apoptotic response, contributing to the decline of apoptosis and the acclimation to chronic stress.