Abstract
Simple SummaryAvian eggs provide huge benefits to both science and society by providing an important model for developmental studies and a high-quality protein source for the human diet. Especially, the hard-shell layer existing at the outer part of eggs is a unique characteristic, which is exclusive in avian species compared to other egg-laying species. Among various avian models developed to investigate genetic factors for potential industrial application, myostatin (MSTN) mutations in quail and chickens were recently generated, resulting in improved meat yield. In addition to previously reported growth and egg production traits in MSTN mutant quail, eggshell quality of mutants was further investigated in this study. Although eggshell height, width, and weight were increased by the MSTN mutation, eggshell breaking strength (EBS) and eggshell thickness were decreased in mutant eggs compared to wild-type eggs. Although these data indicated that decreased eggshell thickness contributed to decreased EBS in mutant eggs, the cellular mechanism of thinner eggshell formation in uterus by MSTN mutation needs to be further investigated using MSTN mutant quail.Recently developed myostatin (MSTN) mutant quail and chickens demonstrated similar effects of MSTN on muscle and fat developments between avian and mammalian species. However, the effect of MSTN mutation on the quality of eggshells, an important avian specific characteristic, has not yet been investigated although egg production traits of mutant quail have been studied. In this study, several parameters for eggshell quality, including eggshell size, eggshell weight, eggshell breaking strength (EBS), and eggshell thickness, were all compared between MSTN mutant and wild-type (WT) eggs. MSTN mutant eggs had greater height and width along with heavier eggshell weight compared to WT eggs, which shows proportional improvement in egg size as affected by the MSTN mutation. However, EBS and eggshell thickness were decreased in mutant eggs compared to WT eggs. In addition, the palisade layer, the thickest and most important layer for the strength of an eggshell, was also decreased without a change in the number of vesicular holes. These data indicated that decreases in the thickness of the eggshell and the palisade layer would be a main factor contributing to a lower EBS in mutant eggs. MSTN mutant quail provide a useful model to better understand the function of MSTN on avian uterine cell development and eggshell biomineralization.
Highlights
The anti-myogenic function of myostatin (MSTN) was discovered from the experiment generating MSTN knockout mice [1] and further demonstrated in other MSTN mutant animals and humans [2,3,4,5,6,7,8,9]
The average sizes of the MSTN mutant eggs were larger, since the height and width of the mutant eggs were significantly increased by approximately 2% and 3%, respectively, compared to those of the WT eggs. (Table 1)
eggshell breaking strength (EBS) was significantly decreased in the MSTN mutant eggs compared to the WT eggs, indicating a weaker eggshell in the MSTN group
Summary
The anti-myogenic function of myostatin (MSTN) was discovered from the experiment generating MSTN knockout mice [1] and further demonstrated in other MSTN mutant animals and humans [2,3,4,5,6,7,8,9]. Since the generation and identification of MSTN mutant mice and cattle [1,2,3], respectively, various mammalian models carrying the MSTN mutation have been developed and identified to investigate MSTN functions in mammals for more than 20 years. Due to MSTN mutant chickens and quail having higher muscle mass and lower fat deposition, the major functions of MSTN on muscle and adipose tissues are conceptually similar between mammalian and avian species. Additional research regarding MSTN functions on avian-specific characteristics is still needed
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