# Multi-Omics Analysis of the Potential Mechanisms of Skin Albinism in Edangered Percocypris pingi: Abnormal Ubiquitination and Calcium Signal Inhibition

## TL;DR

This study explores the causes of skin albinism in an endangered fish species, revealing how protein breakdown and calcium signaling issues lead to pigment loss.

## Contribution

The study reveals novel synergistic mechanisms involving ubiquitination and calcium signaling inhibition in fish albinism.

## Key findings

- Hyperactivation of ubiquitin-mediated proteolysis suppresses TYR/TYRP1 activity and disrupts melanosome pH homeostasis.
- Inhibition of calcium signaling impairs melanin transport in albino P. pingi.
- These mechanisms synergistically drive pigment loss in the endangered fish species.

## Abstract

Percocypris pingi is an endangered protected fish species in China. Its albino variants exhibit growth retardation and physiological abnormalities. Understanding its albinism mechanism holds significant scientific importance for molecular breeding programs and disease model development. This study integrated transcriptomic and proteomic analyses, combined with histopathological and molecular biological techniques, to systematically compare molecular differences in skin tissues between albino and wild-type P. pingi, with a focus on elucidating the multidimensional regulatory mechanisms underlying skin albinism. Our findings suggest that albinism in P. pingi is synergistically driven by hyperactivation of ubiquitin-mediated proteolysis (which suppressed TYR/TYRP1 enzymatic activity and disrupted the pH homeostasis of melanosomes), and inhibition of calcium signaling (which impeded melanin transport). This discovery provides novel insights into the mechanisms of pigment loss in fish species and offers a valuable reference for molecular breeding of endangered species as well as research on pigmentation-related disorders.