Hansen Peter J
Department of Animal Sciences, D. H. Barron Reproductive and Perinatal Biology Research Program, and Genetics Institute, University of Florida, Gainesville, FL 32611-0910, USA. Email:
Reprod Fertil Dev. 2014 Dec;27(1):22-30. doi: 10.1071/RD14311.
Reproduction is among the physiological functions in mammals most susceptible to disruption by hyperthermia. Many of the effects of heat stress on function of the oocyte and embryo involve direct effects of elevated temperature (i.e. heat shock) on cellular function. Mammals limit the effects of heat shock by tightly regulating body temperature. This ability is genetically controlled: lines of domestic animals have been developed with superior ability to regulate body temperature during heat stress. Through experimentation in cattle, it is also evident that there is genetic variation in the resistance of cells to the deleterious effects of elevated temperature. Several breeds that were developed in hot climates, including Bos indicus (Brahman, Gir, Nelore and Sahiwal) and Bos taurus (Romosinuano and Senepol) are more resistant to the effects of elevated temperature on cellular function than breeds that evolved in cooler climates (Angus, Holstein and Jersey). Genetic differences are expressed in the preimplantation embryo by Day 4-5 of development (after embryonic genome activation). It is not clear whether genetic differences are expressed in cells in which transcription is repressed (oocytes >100 µm in diameter or embryos at stages before embryonic genome activation). The molecular basis for cellular thermotolerance has also not been established, although there is some suggestion for involvement of heat shock protein 90 and the insulin-like growth factor 1 system. Given the availability of genomic tools for genetic selection, identification of genes controlling cellular resistance to elevated temperature could be followed by progress in selection for those genes within the populations in which they exist. It could also be possible to introduce genes from thermotolerant breeds into thermally sensitive breeds. The ability to edit the genome makes it possible to design new genes that confer protection of cells from stresses like heat shock.
生殖是哺乳动物最易受高温干扰的生理功能之一。热应激对卵母细胞和胚胎功能的许多影响涉及温度升高(即热休克)对细胞功能的直接影响。哺乳动物通过严格调节体温来限制热休克的影响。这种能力受基因控制:已经培育出在热应激期间调节体温能力更强的家畜品系。通过对牛的实验也明显看出,细胞对高温有害影响的抗性存在基因变异。在炎热气候下培育的几个品种,包括印度瘤牛(婆罗门牛、吉尔牛、尼尔罗牛和萨希瓦尔牛)和普通牛(罗莫辛努阿牛和塞内波尔牛),比在较凉爽气候下进化的品种(安格斯牛、荷斯坦牛和泽西牛)对高温对细胞功能的影响更具抗性。在发育的第4 - 5天(胚胎基因组激活后),植入前胚胎中就会表现出基因差异。目前尚不清楚在转录受到抑制的细胞(直径大于100 µm的卵母细胞或胚胎基因组激活前阶段的胚胎)中是否会表现出基因差异。尽管有一些迹象表明热休克蛋白90和胰岛素样生长因子1系统参与其中,但细胞耐热性的分子基础尚未确立。鉴于有用于基因选择的基因组工具,确定控制细胞对高温抗性的基因后,就可以在存在这些基因的种群中对这些基因进行选择。也有可能将耐热品种的基因导入热敏品种。基因组编辑能力使得设计新基因成为可能,这些新基因能保护细胞免受热休克等应激影响。