Comparative analysis of testis transcriptomes associated with male infertility in cattleyak

Cattleyak exhibit equivalent adaptability to harsh environment, as yak and much higher performances than yak. However, male infertility of cattleyak due to spermatogenic arrest greatly restricts their effective utilization in yak breeding. Although much work has been done to investigate the mechanisms of spermatogenic arrest, there is little information available in regard to the differences in transcriptomic profiling between cattleyak and yak testes. In this work, histologic observation indicated that spermatogonia were the main type of germ cells present in cattleyak testis, whereas all types of germ cells in differentiation were present in yak testis. Transcriptomic profiling identified 2960 differentially expressed genes (DEGs) in which 679 were upregulated and 2281 were downregulated in cattleyak. Significantly enriched gene ontology terms comprised a large number of DEGs associated with male infertility of cattleyak. The upregulation of STRA8 and NLRP14 may be associated with the accumulation of undifferentiated spermatogonial cells and serious cellular apoptosis in cattleyak. However, downregulated SPP1, SPIN2B, and PIWIL1 were associated with cell cycle progression and spermatogonial genome integrity, whereas CDKN2C, CYP26A1, OVOLI, GGN, MAK, INSL6, RNF212, TSSKIB, TSSIQ, and TSSK6 were involved in meiosis. Furthermore, scores of genes associated with sperm components were also downregulated in cattleyak. Wnt/beta-catenin signaling pathway was involved in the top-listed three significantly enriched pathways, and the downregulation of Wnt3a, PP2A, and TCF/LEF-1 may have contributed to the arrest of spermatogonial differentiation in cattleyak. The data suggest that spermatogenic arrest of cattleyak might occur at the stage of spermatogonial differentiation and get aggravated during meiosis, which results in minimal number of sperms with morphologic abnormalities and structural deficiency lacking fertilization ability. (C) 2016 Elsevier Inc. All rights reserved.