Troponin T isoform expression is modulated during Atlantic Halibut metamorphosis

Abstract

BackgroundFlatfish metamorphosis is a thyroid hormone (TH) driven process which leads to a dramatic change from a symmetrical larva to an asymmetrical juvenile. The effect of THs on muscle and in particular muscle sarcomer protein genes is largely unexplored in fish. The change in Troponin T (TnT), a pivotal protein in the assembly of skeletal muscles sarcomeres and a modulator of calcium driven muscle contraction, during flatfish metamophosis is studied.ResultsIn the present study five cDNAs for halibut TnT genes were cloned; three were splice variants arising from a single fast TnT (fTnT) gene; a fourth encoded a novel teleost specific fTnT-like cDNA (AfTnT) expressed exclusively in slow muscle and the fifth encoded the teleost specific sTnT2. THs modified the expression of halibut fTnT isoforms which changed from predominantly basic to acidic isoforms during natural and T4 induced metamorphosis. In contrast, expression of red muscle specific genes, AfTnT and sTnT2, did not change during natural metamorphosis or after T4 treatment. Prior to and after metamorphosis no change in the dorso-ventral symmetry or temporal-spatial expression pattern of TnT genes and muscle fibre organization occurred in halibut musculature.ConclusionMuscle organisation in halibut remains symmetrical even after metamorphosis suggesting TH driven changes are associated with molecular adaptations. We hypothesize that species specific differences in TnT gene expression in teleosts underlies different larval muscle developmental programs which better adapts them to the specific ecological constraints.

What determines growth potential and juvenile quality of farmed fish species?

“…; Campinho et al . ). Moreover, the whole genome duplication at the base of the teleost radiation, followed by additional duplication events in other lineages such as the salmonids, created multiple copies of genes involved in muscle growth pathways, increasing the potential flexibility of growth regulation in teleosts compared with mammals.…”

“…By the early larval stage a resident population of Pax7 expressing myogenic precursor cells is evident throughout the myotome and these cells are thought to fuel the dramatic increase in muscle mass during ontogeny. In several marine species, the larval germinal zones are evident at around the onset of first swim and are generally depleted during metamorphosis or in the period shortly after (Galloway et al 1999a,b;Campinho et al 2007;Silva et al 2010). The first attempts of the larvae at cruise swimming in search of food are extremely important for their survival at that age, but there is no trend in the timing of stratified hyperplasia (SH) in relation to the onset of exogenous feeding (Table 1): in gilthead sea bass, sea bream, red sea bream, halibut and cod hyperplastic growth seems to be triggered by endogenous energy sources, as a preparation for rapid growth after the onset of exogenous feeding Galloway et al 1999a,b;Alami-Durante et al 2006).…”

Troponin T isoforms and posttranscriptional modifications: Evolution, regulation and function

“…While the intron-less nature of fish slow TnT gene precludes alternative splicing, natural and thyroid hormone-induced metamorphosis of Atlantic halibut is accompanied by switches of fast TnT from predominantly larger acidic isoforms to smaller basic isoforms via alternative splicing in the N-terminal variable region (131). …”

Involvement of growth hormone-insulin-like growth factor I system in cranial remodeling during halibut metamorphosis as indicated by tissue- and stage-specific receptor gene expression and the presence of growth hormone receptor protein

“…During metamorphosis, the skin (Campinho et al 2007b), gastrointestinal system (Miwa et al 1992), nervous system (Osse and Van den Boogaart 1997), musculo-skeletal system (Campinho et al 2007a;Saele et al 2006), and osmoregulatory tissues (see Schreiber 2001) undergo major changes. In Atlantic halibut (Hippoglossus hippoglossus), migration of the ethmoid plate toward the ocular side and subsequent remodeling of the frontal plate together with fibroblast proliferation are suggested to drive eye migration, a major event leading to asymmetry (Saele et al 2006).…”