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In recent years, flathead grey mullets (Mugil cephalus) cultured in Eilat (Israel) have been highly affected by Vibrio harveyi, showing neurological signs such as uncoordinated circular swimming followed by high mortality rates. Despite the advances in and different approaches to control vibriosis associated with Vibrio harveyi, including commercial vaccines, most of them have not succeeded in long-term protection. In this study, we evaluated the effectiveness, long-term protection, and antibody production of three vaccine preparations: heat-killed bacteria (HKB), membrane proteins denaturation (BME PROT), and internal proteins (INT PROT) developed specifically against Vibrio harveyi for grey mullets. Our results show that fish immunized with heat-killed bacteria emulsified with adjuvant presented the most effective and long-lasting protection against the bacterium, and a cross-protection against other bacteria from the harveyi clade. The effectiveness of each immunization treatment correlated with the levels of specific antibody production against Vibrio harveyi in the serum of the immunized fish. [ABSTRACT FROM AUTHOR]

The grey mullet is a catadromous species that spawns in the taurine-rich seawater environment, followed by the young fish generally migrating to less saline, low taurine waters during the larva-juvenile transition. Consequently, this study aimed to (1) determines whether there is a dietary taurine requirement in juvenile grey mullet for enhanced growth and (2) the potential for taurine biosynthesis. The experimental system consisted of sixteen 400-l V-tanks, where filtered, UV-treated ambient seawater (40 °) entered the bottom of the tanks at a rate of 7 tank exchanges/day. This allowed the testing of four 1 mm pelleted diets (0, 0.5, 1.0, and 2.0% taurine DW diet) in replicates of 4 tanks/treatment for 58 days. Grey mullet juveniles demonstrated (P<0.05) a specific requirement for a 0.5% taurine DW diet for improved growth. Fish fed the taurine diets displayed populations with a markedly (P < 0.05) higher average number of surviving fish (23.4±1.1) of moderately sized (10-20 g) cohorts than smaller (< 10 g) individuals (12.5±1.1). In contrast, the fish fed the taurine control (0% taurine) exhibited similar average numbers of small and moderate sized fish (18.0±3.6-20.0±4.1). Dietary taurine accumulated highly (P<0.05) in the muscles in a dose dependent manner but less so (P<0.05) in eyes, and liver. The gene expression of liver cysteine sulfinic acid decarboxylase (CSD) exhibited an upregulation (P<0.05) with taurine diets from 0 to 1% but was down regulated (P<0.05) in fish fed the 2% taurine DW diet. [ABSTRACT FROM AUTHOR]

Various master key regulators (MKRs) that control a binary switch of sex determination (SD) have been found in fish; these provide an excellent model for the study of vertebrate genetic SD. The SD region in flathead grey mullet has been previously mapped to a 1 Mbp region harboring 27 genes, of which one is follicle-stimulating hormone receptor (fshr). Although this gene is involved in gonad differentiation and function, it has not been considered as an MKR of SD. We systematically investigated polymorphism in mullet fshr using DNA shotgun sequences, and compared them between males and females. Capable of encoding nonconservative amino acid substitutions, c.1732G>A and c.1759T>G exhibited association with sex on a population level (N = 83; P 6.7×10-19). Hence, 1732 A and 1759 G represent a male-specific haplotype of the gene, designated as "fshry." Additional flanking SNPs showed a weaker degree of association with sex, delimiting the SD critical region to 143 nucleotides on exon 14. Lack of homozygotes for fshry, and the resulting divergence from Hardy- Weinberg equilibrium (N = 170; P 3.9 ×10-5 ), were compatible with a male heterogametic model (XY/XX). Capable of replacing a phenylalanine with valine, c.1759T>G alters a conserved position across the sixth transmembrane domain of vertebrate FSHRs. Amino acid substitutions in this position in vertebrates are frequently associated with constant receptor activation and consequently with FSH/FSHR signaling alteration; thus, indicating a potential role of fshr as an MKR of SD [ABSTRACT FROM AUTHOR]