Abstract
BackgroundThe mechanism of body growth in mammals is poorly understood. Here, we investigated the regulatory networks involved in body growth through transcriptomic analysis of pituitary and epiphyseal tissues of smaller sized Debao ponies and Mongolian horses at the juvenile and adult stages.ResultsWe found that growth hormone receptor (GHR) was expressed at low levels in long bones, although growth hormone (GH) was highly expressed in Debao ponies compared with Mongolian horses. Moreover, significant downregulated of the GHR pathway components m-RAS and ATF3 was found in juvenile ponies, which slowed the proliferation of bone osteocytes. However, WNT2 and PLCβ2 were obviously upregulated in juvenile Debao ponies, which led to premature mineralization of the bone extracellular matrix. Furthermore, we found that the WNT/Ca2+ pathway may be responsible for regulating body growth. GHR was demonstrated by q-PCR and Western blot analyses to be expressed at low levels in long bones of Debao ponies. Treatment with WNT antagonistI decreased the expression of WNT pathway components (P < 0.05) in vitro. Transduction of ATDC5 cells with a GHR-RNAi lentiviral vector decreased the expression of the GHR pathway components (P < 0.05). Additionally, the expression of the IGF-1 gene in the liver was lower in Debao ponies than in Mongolian horses at the juvenile and adult stages. Detection of plasma hormone concentrations showed that Debao ponies expressed higher levels of IGF-1 as juveniles and higher levels of GH as adults than Mongolian horses, indicating that the hormone regulation in Debao ponies differs from that in Mongolian horses.ConclusionOur work provides insights into the genetic regulation of short stature growth in mammals and can provide useful information for the development of therapeutic strategies for small size.
Highlights
The mechanism of body growth in mammals is poorly understood
Debao pony (DP) exhibited no significant differences in height between the juveniles and adults stages, while Mongolian horse (MH) did exhibit significant differences in height
We constructed and sequenced an RNA-seq library from 24 samples of pituitary and epiphyseal tissues taken from three DPs and three MHs at the juvenile and adult stages (Fig. 1a), as these tissue types are related to body size development [12, 13]
Summary
The mechanism of body growth in mammals is poorly understood. Here, we investigated the regulatory networks involved in body growth through transcriptomic analysis of pituitary and epiphyseal tissues of smaller sized Debao ponies and Mongolian horses at the juvenile and adult stages. Whole-genome sequence analysis has shown that the genetic architecture of stature in cattle is similar to that in humans [7]. A few studies on the genetic aspects of body size in horses have been conducted. A genome-wide association study based on SNPs identified two chromosomal loci near the LCORL/NCAPG gene and the ZFAT gene that have already been shown to influence body height in humans [9]. A complementary genome analysis of ponies and tall horses identified the genomic loci related to body height and metabolic traits and discovered that HMGA2 c.83G > A (p.G28E) variants were significantly altered in Welsh ponies, suggesting that the highly related loci in the ponies were highly efficient in altering metabolic pathways [11]. The molecular pathways regulating body height in horses remain unclear
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
