FGF- and SHH-based molecular signals regulate barbel and craniofacial development in catfish.

BACKGROUND: Catfish (Siluriformes) are characterized by unique morphologies, including enlarged jaws with movable barbels and taste buds covering the entire body surface. Evolution of these characteristics was a crucial step in their adaptive radiation to freshwater environments. However, the developmental processes of the catfish craniofacial region and taste buds remain to be elucidated; moreover, little is known about the molecular mechanisms underlying the morphogenesis of these structures. RESULTS: In Amur catfish (Silurus asotus), three pairs of barbel primordia are formed by 2 days post-fertilization (dpf). Innervation of the peripheral nerves and formation of muscle precursors are also established during early development. Taste buds from the oral region to the body trunk are formed by 4 dpf. We then isolated catfish cognates Shh (SaShh) and Fgf8 (SaFgf8), which are expressed in maxillary barbel primordium at 1-2 dpf. Further, SHH signal inhibition induces reduction of mandibular barbels with abnormal morphology of skeletal elements, whereas it causes no apparent abnormality in the trigeminal and facial nerve morphology. We also found that mandibular barbel lengths and number of taste buds are reduced by FGF inhibition, as seen in SHH signal inhibition. However, unlike with SHH inhibition, the abnormal morphology of the trigeminal and facial nerves was observed in FGF signal-inhibited embryos. CONCLUSION: The developmental processes of Amur catfish are consistent with those reported for other catfish species. Thus, developmental aspects of craniofacial structures and taste buds may be conserved in Siluriformes. Our findings also suggest that SHH signaling plays a crucial role in the formation of barbels and taste buds, without affecting nerve projection, while FGF signaling is required for the development of barbels, taste buds, and branchial nerves. Thus, SHH and FGF signaling plays key roles in the ontogenesis and evolution of some catfish-specific characteristics.

Nervous system disruption and swimming abnormality in early-hatched pufferfish (Takifugu niphobles) larvae caused by pyrene is independent of aryl hydrocarbon receptors.

Pyrene, a member of the polycyclic aromatic hydrocarbons (PAHs), contributes to abnormality in the size of the brain and the swimming behavior of pufferfish (Takifugu niphobles) larvae. We hypothesized that the aryl hydrocarbon receptor (AHR) may mediate pyrene-induced toxic effects because AHR is assumed to be a candidate for the downstream target of PAHs in many cases. To identify the contribution of AHR on developing pufferfish, we performed exposure experiments using ß-naphthoflavone, an agonist of AHR. We found that the toxic effects of pyrene and ß-naphthoflavone in pufferfish larvae are fundamentally different. Pyrene specifically induced problems in the developing midbrain and in swimming behavior, while ß-naphthoflavone affected the heartbeat rate and the size of the yolk. These results suggest that the behavioral and morphological abnormality caused by pyrene exposure is mediated by an AHR-independent pathway. Alternatively, defects caused by pyrene may be attributed to the inhibition of the FGF signal.

Involvement of Slit-Robo signaling in the development of the posterior commissure and concomitant swimming behavior in Xenopus laevis.

INTRODUCTION: During vertebrate development, the central nervous system (CNS) has stereotyped neuronal tracts (scaffolds) that include longitudinal and commissural axonal bundles, such as the medial longitudinal fascicle or the posterior commissure (PC). As these early tracts appear to guide later-developing neurons, they are thought to provide the basic framework of vertebrate neuronal circuitry. The proper construction of these neuronal circuits is thought to be a crucial step for eliciting coordinated behaviors, as these circuits transmit sensory information to the integrative center, which produces motor commands for the effective apparatus. However, the developmental plan underlying some commissures and the evolutionary transitions they have undergone remain to be elucidated. Little is known about the role of axon guidance molecules in the elicitation of early-hatched larval behavior as well. RESULTS: Here, we report the developmentally regulated expression pattern of axon-guidance molecules Slit2 ligand and Robo2 receptor in Xenopus laevis and show that treatment of X. laevis larvae with a slit2- or robo2-morpholino resulted in abnormal swimming behavior. We also observed an abnormal morphology of the PC, which is part of the early axonal scaffold. CONCLUSION: Our present findings suggest that expression patterns of Slit2 and Robo2 are conserved in tetrapods, and that their signaling contributes to the construction of the PC in Xenopus. Given that the PC also includes several types of neurons stemming from various parts of the CNS, it may represent a candidate prerequisite neuronal tract in the construction of subsequent complex neuronal circuits that trigger coordinated behavior.

Pyrene induces a reduction in midbrain size and abnormal swimming behavior in early-hatched pufferfish larvae.

Spills of heavy oil (HO) have an adverse effect on marine life. We have demonstrated previously that exposure to HO by fertilized eggs of the pufferfish (Takifugu rubripes) induces neural disruption and behavioral abnormality in early-hatched larvae. Here, two kinds of polycyclic aromatic hydrocarbons, pyrene and phenanthrene, were selected to examine their toxic effects on larval behavior of another pufferfish species (T. niphobles). Larvae exposed to pyrene or phenanthrene exhibited no abnormalities in morphology. However, those exposed to pyrene but not phenanthrene swam in an uncoordinated manner, although their swimming distance and speed were normal. The optic tectum, a part of the midbrain, of pyrene-exposed larvae did not grow to full size. Thus, these findings are indicated that pyrene might be a contributor to the behavioral and neuro-developmental toxicity, although there is no indication that it is the only compound participating in the toxicity of the heavy oil mixture.