A fisherman's new tale: Nutrient-mediated mechanisms of brachial plasticity in rainbow trout.

点击翻译按钮获取中文摘要

Phosphorus (P) plays a vital physiological role in intermediary metabolism, and is a key component of DNA/RNA, phospholipids, and skeletal tissues. Despite these key roles, little is known about the physiological effects of P deficiency. There have been a number of studies demonstrating dietary regulation of Pi transport in fish and the regulation of Pi absorption in vivo. In rainbow trout, dietary P restriction increases intestinal Pi uptake due to a number of molecular mechanisms regulating Pi transport. Dietary P restriction has been shown to upregulate both mRNA species as well as to increase Pi uptake by the tissue. Sodium-NaPi is a Pi transporter found in kidney, and is upregulated by dietary P restriction, although recent work has suggested that renal NaPi mRNA is relatively insensitive to changes in dietary P due to the fact that he primary mechanism of renal P regulation is mediated by the trafficking of NaPi protein that is independent of gene transcription. Recent work from my laboratory demonstrates that P-deficient rainbow trout are able to take up P from non feed-derived P. Experiments have consistently revealed that P-deficient fish from surrounding water. We propose a variety of approaches to verify uptake of P from the water by P-deficient fish. We will confirm the uptake of P, and this phenomenon will be characterized, localised using immuno-histological localisation and next generation sequencing techniques/qPCR employed to determine the key pathways that are affected to permit P uptake. The dynamics of the proposed phenomenon and the impact of fish size, P status will be studied. This work will have an important impact on the understanding of the effect of nutrient absorption during nutrient deficiency development, and in particular the adaptive response of freshwater trout to fundamentally alter physiological processes that are currently thought to be insignificant.