Abstract
The expression of testicular genes following acute heat stress has been reported in layer-type roosters, but few similar studies have been conducted on broilers. This study investigated the effect of acute heat stress on the gene expression in the testes of a broiler-type strain of Taiwan country chickens. Roosters were subjected to acute heat stress (38°C) for 4 h, and then exposed to 25°C, with testes collected 0, 2, and 6 h after the cessation of heat stress, using non-heat-stressed roosters as controls (n = 3 roosters per group). The body temperature and respiratory rate increased significantly (p<0.05) during the heat stress. The numbers of apoptotic cells increased 2 h after the acute heat stress (79 ± 7 vs. 322 ± 192, control vs. heat stress; p<0.05), which was earlier than the time of increase in layer-type roosters. Based on a chicken 44 K oligo microarray, 163 genes were found to be expressed significantly different in the testes of the heat-stressed chickens from those of the controls, including genes involved in the response to stimulus, protein metabolism, signal transduction, cell adhesion, transcription, and apoptosis. The mRNA expressions of upregulated genes, including HSP25, HSP90AA1, HSPA2, and LPAR2, and of downregulated genes, including CDH5, CTNNA3, EHF, CIRBP, SLA, and NTF3, were confirmed through quantitative real-time polymerase chain reaction (qRT-PCR). Moreover, numerous transcripts in the testes exhibited distinct expressions between the heat-stressed broiler-type and layer-type chickens. We concluded that the transcriptional responses of testes to acute heat stress may differ between the broiler-type and layer-type roosters. Whether the differential expression patterns associate with the heat-tolerance in the strains require a further exploration.
Highlights
A high ambient temperature impairs spermatogenesis and leads to low fertility through a decline of the sperm count, motility, and fertilization rate, as well as an elevation of abnormal cells in domestic animals [1,2,3]
The results suggested that genes participating in signal transduction were upregulated, including the lysophosphatidic acid receptor 2 (LPAR2), or downregulated, including the interleukin 13 receptor, alpha 1 (IL13RA1), in the testes of B-strain Taiwan country chickens (TCCs) after heat stress
The functional network analysis revealed that genes of heat-shock proteins (HSPs) and cochaperones (HSP70, HSP90AA1, heat-shock protein 25 (HSP25), and DNAJA4) as well as antiapoptotic BCL2-associated athanogene 3 (BAG3) and SERPINB2 were upregulated in heat-stressed chicken testes
Summary
A high ambient temperature impairs spermatogenesis and leads to low fertility through a decline of the sperm count, motility, and fertilization rate, as well as an elevation of abnormal cells in domestic animals [1,2,3]. To understand the adverse effect of high temperature on spermatogenesis, cellular and molecular mechanisms in response to heat stress have been studied [4,5,6,7,8]. Overproduced radical oxygen species that is induced through heat stress has been shown to cause oxidative stress and lead to apoptosis in spermatogenic cells, in spermatocytes [4,7]. A microarray was used to explore the expressions of testicular genes in mouse testes, and the expression levels of genes associated with DNA repair and recombination, protein synthesis, protein folding, and cell cycle reduced after heat stress [5]. The expressions of heatshock protein family genes were augmented against heat stress in mouse testes. Kim et al [8] argued that multiple mechanisms were involved in heat-shock-induced subfertility or infertility
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