Agouti-Signalling Protein Overexpression Reduces Aggressiveness in Zebrafish

Feeding motivation plays a crucial role in food intake and growth. It closely depends on hunger and satiation, which are controlled by the melanocortin system. Overexpression of the inverse agonist agouti-signalling protein (ASIP) and agouti-related protein (AGRP) leads to enhanced food intake, linear growth, and weight. In zebrafish, overexpression of Agrp leads to the development of obesity, in contrast to the phenotype observed in transgenic zebrafish that overexpress asip1 under the control of a constitutive promoter (asip1-Tg). Previous studies have demonstrated that asip1-Tg zebrafish exhibit larger sizes but do not become obese. These fish display increased feeding motivation, resulting in a higher feeding rate, yet a higher food ration is not essential in order to grow larger than wild-type (WT) fish. This is most likely attributed to their improved intestinal permeability to amino acids and enhanced locomotor activity. A relationship between high feeding motivation and aggression has been previously reported in some other transgenic species showing enhanced growth. This study aims to elucidate whether the hunger observed in asip1-Tg is linked to aggressive behaviour. Dominance and aggressiveness were quantified using dyadic fights and mirror-stimulus tests, in addition to the analysis of basal cortisol levels. The results indicate that asip1-Tg are less aggressive than WT zebrafish in both dyadic fights and mirror-stimulus tests.

This study was financed by funds from MCIN/AEI/10.13039/501100011033 (PID2019-103969RB-C33 and PID2022-136288OB-C33 to J.M.C.-R.) and, as appropriate, by “ERDF A Way of Making Europe,” by the “European Union,” or by the “European Union Next Generation EU/PRTR.” This study forms part of the ThinkInAzul programme and was supported by MCIN with funding from the European Union NextGenerationEU (PRTR-C17.I1) and by the Generalitat Valenciana (THINKINAZUL/2021/025). A.G.-G. was financed thanks to a predoctoral fellowship (FPI) from AEI code: BES-2017-082424.

Peer reviewed