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Published on: August 15, 2011
The influence of mouse Ped gene expression on postnatal development
Adam Watkins1, Adrian Wilkins, Clive Osmond
1School of Biological Sciences, Developmental and Cell Biology Group, University of Southampton, Bassett Crescent East, Southampton SO16 7PX, UK. ajw7@soton.ac.uk
Insights
The Ped gene influences preimplantation embryo development rate, affecting postnatal growth and cardiovascular function. Mice with slower development (Ped slow) showed increased body weight and higher blood pressure later in life.
Area of Science:
- Genetics
- Developmental Biology
- Physiology
Background:
- The Ped (preimplantation embryo development) gene encodes Qa-2 protein, influencing early embryonic development rates.
- A faster preimplantation development (Ped fast) phenotype is associated with Qa-2 protein expression, while its absence leads to a slower (Ped slow) phenotype.
Purpose of the Study:
- To investigate the impact of Ped gene expression on postnatal growth, systolic blood pressure, and organ allometry.
- To compare the physiological outcomes between mice with differing Ped gene expression levels.
Main Methods:
- Utilized two congenic mouse strains: B6.K1 (Ped slow; Qa-2 negative) and B6.K2 (Ped fast; Qa-2 positive).
- Monitored postnatal growth, measured systolic blood pressure at 21 weeks, and analyzed organ-to-body weight ratios.
Main Results:
- B6.K1 mice were lighter at birth but became heavier postnatally compared to B6.K2 mice.
- B6.K1 mice exhibited elevated systolic blood pressure and increased serum angiotensin-converting enzyme (ACE) activity.
- Altered organ:body weight ratios were observed, notably higher lung ratios in B6.K1 females.
Conclusions:
- Ped gene expression rate correlates with postnatal growth trajectories.
- Early embryonic development rate is associated with later-life cardiovascular function and ACE activity.
- Findings suggest a link between preimplantation development and adult physiological characteristics.
Abstract:
The Ped (preimplantation embryo development) gene, whose product is Qa-2 protein, is correlated with a faster rate of preimplantation development (Ped fast phenotype) in mice that express Qa-2 protein compared with mice with an absence of Qa-2 protein (Ped slow phenotype). In the current study, we have used two congenic mouse strains differentially expressing the Ped gene, strain B6.K1 (Ped slow; Qa-2 negative) and strain B6.K2 (Ped fast; Qa-2 positive), to investigate the effects of Ped gene expression on postnatal growth profiles, systolic blood pressure and adult organ allometry. At birth, B6.K1 mice were moderately lighter than B6.K2 mice. B6.K1 mice became heavier during postnatal life (P < 0.05) and had elevated systolic blood pressure at 21 weeks of age when compared with B6.K2 mice (P = 0.006). B6.K1 mice also demonstrated elevated serum angiotensin-converting enzyme (ACE) activity, a known regulator of blood pressure (P = 0.037). Altered organ:body weight ratios were also observed, with the B6.K1 females having a higher ratio for lungs than B6. K2 females (P = 0.014). These data provide evidence of an association between the rate of preimplantation embryo development, postnatal growth and later cardiovascular function.

