Uterine structure and function contributes to the formation of the sandpaper-shelled eggs in laying hens.

The avian eggshell is formed in the uterus, and eggshell quality usually decreases markedly in the late phase of hen laying cycles. Production of sandpaper-shelled eggs (SE), a category of eggs with relatively less eggshell quality, causes a great economic loss. Underlying mechanisms of SE formation, however, remain unclear. For the present study, it was hypothesized that alterations in uterine structure and function contribute to SE formation. To test this hypothesis, uterine samples were collected from 450-day-old hens that produced normal eggs (NE) and SE (based on 2-week-long assessments, n = 10) for histomorphological and transcriptome analyses. Compared with the NE group, uteri of the SE group were apparently atrophied. Furthermore, a total of 211 differentially expressed genes (DEGs) were identified in the uteri of hens of the two groups. These DEGs were clustered into 145 gene ontology terms (FDR < 0.05) and enriched in 12 KEGG pathways (P < 0.10), which are primarily related to organ morphogenesis and development, cell growth, differentiation and death, ion transport, endocrine and cell communication, immune response, and corticotropin-releasing hormones. In particular, corticotropin may be an important factor in SE formation because of effects on ion transport. Furthermore, as indicated by lesser abundances of relevant mRNA transcripts, the lesser expression of genes related to ion transport and matrix proteins also contribute to SE production because of effects on eggshell formation. In conclusion, results from this study revealed there were structural and functional differences in the hen uterus in NE and SE groups.