Tate Kevin B, Rhen Turk, Eme John, Kohl Zachary F, Crossley Janna, Elsey Ruth M, Crossley Dane A
Department of Biology, McMaster University, Hamilton, Ontario, Canada;
Department of Biology, University of North Dakota, Grand Forks, North Dakota;
Am J Physiol Regul Integr Comp Physiol. 2016 Jun 1;310(11):R1267-78. doi: 10.1152/ajpregu.00320.2015. Epub 2016 Apr 13.
During embryonic development, environmental perturbations can affect organisms' developing phenotype, a process known as developmental plasticity. Resulting phenotypic changes can occur during discrete, critical windows of development. Critical windows are periods when developing embryos are most susceptible to these perturbations. We have previously documented that hypoxia reduces embryo size and increases relative heart mass in American alligator, and this study identified critical windows when hypoxia altered morphological, cardiovascular function and cardiac gene expression of alligator embryos. We hypothesized that incubation in hypoxia (10% O2) would increase relative cardiac size due to cardiac enlargement rather than suppression of somatic growth. We exposed alligator embryos to hypoxia during discrete incubation periods to target windows where the embryonic phenotype is altered. Hypoxia affected heart growth between 20 and 40% of embryonic incubation, whereas somatic growth was affected between 70 and 90% of incubation. Arterial pressure was depressed by hypoxic exposure during 50-70% of incubation, whereas heart rate was depressed in embryos exposed to hypoxia during a period spanning 70-90% of incubation. Expression of Vegf and PdgfB was increased in certain hypoxia-exposed embryo treatment groups, and hypoxia toward the end of incubation altered β-adrenergic tone for arterial pressure and heart rate. It is well known that hypoxia exposure can alter embryonic development, and in the present study, we have identified brief, discrete windows that alter the morphology, cardiovascular physiology, and gene expression in embryonic American alligator.
在胚胎发育过程中，环境扰动会影响生物体的发育表型，这一过程称为发育可塑性。由此产生的表型变化可能发生在发育的离散关键期。关键期是发育中的胚胎对这些扰动最敏感的时期。我们之前记录了缺氧会减小美国短吻鳄胚胎的大小并增加相对心脏质量，并且本研究确定了缺氧改变短吻鳄胚胎形态、心血管功能和心脏基因表达的关键期。我们假设在缺氧（10%氧气）环境中孵化会由于心脏增大而不是抑制体细胞生长导致相对心脏大小增加。我们在离散的孵化期将短吻鳄胚胎暴露于缺氧环境中，以针对胚胎表型发生改变的时期。缺氧在胚胎孵化的20%至40%期间影响心脏生长，而体细胞生长在孵化的70%至90%期间受到影响。在孵化的50%至70%期间，缺氧暴露会降低动脉压，而在孵化70%至90%期间暴露于缺氧环境的胚胎心率会降低。在某些缺氧暴露的胚胎处理组中，Vegf和PdgfB的表达增加，并且孵化末期的缺氧改变了动脉压和心率的β-肾上腺素能张力。众所周知，缺氧暴露会改变胚胎发育，在本研究中，我们确定了改变美国短吻鳄胚胎形态、心血管生理学和基因表达的短暂、离散时期。
