Reproductive Biology of the Laboratory Mouse

Pritchett, Kathleen; Taft, Robert A.

doi:10.1016/b978-012369454-6/50057-1

Cited by 24 publications

(26 citation statements)

References 273 publications

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“…Other studies did not find lower nursing time in B6 mice; the difference may be that Brown et al (1999) removed pups from the nest daily for 1-h prior to a retrieval task, and this invasive procedure differentially affected B6 and D2 mice (see discussion by van der Veen et al 2008). Pup mortality can increase with the common environmental stresses of animal husbandry (Pritchett and Taft 2007), and female D2 and B6 mice show a variety of different behavioral responses to stress (Mineur et al 2006). Future studies should investigate whether differential sensitivity of maternal behavior to stress could explain strain differences in mortality.…”

Section: Discussionmentioning

confidence: 93%

Genetic and Maternal Effects on Offspring Mortality in Mice

et al. 2011

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Trade-offs occur when two traits have opposing fitness effects such that positive selection on one trait is constrained by the negative fitness consequences of the other trait. To understand why trade-off may arise we need to study the genetic and non-genetic factors that influence associated traits because these may respond differently to selective pressure. Research into trade-offs has largely focused on the genetic basis of associated traits, yet both maternal effects and epigenetic effects have recently been shown to affect life history traits that play a role in tradeoffs. In this study, we analyze genetic, epigenetic and lifehistory predictors of one of the most important trade-offs, that between offspring number and offspring mortality. Using a large-scale 3-generational intercross between two divergent mouse lines C57BL/6J and DBA/2J, we show that litter size differences between these lines, although significant, are surprisingly not the most important predictors of mortality. Offspring genotype, maternal effects and their interactions are the most influential factors determining mortality. We found significant paternal effects suggesting an important influence of paternal care or potentially the role of imprinted genes. Perhaps contrary to expectations our results further show that the trade-off between offspring number and mortality is not just a simple function of the two factors yielding, on average, an 'optimal' litter size at weaning. Indeed if one focused on litter size and mortality alone, the slope of relationship is the same for the two lines, yet they differ in the number of young at weaning. Our study reveals that a perceived tradeoff between two traits is governed by a more complex set of interactions between genetic and non-genetic effects.

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Section: Discussionmentioning

confidence: 93%

Genetic and Maternal Effects on Offspring Mortality in Mice

et al. 2011

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“…Consistent with these studies, we found that the subset of hilar Prox1-ir cells that are mature GCs (i.e., they express NeuN) increases between PND30 and PND60, suggesting a preferential increase in mature GCs. These changes may be related to puberty, which begins at approximately PND30 in the rodent, and ends at approximately PND50 (Pritchett and Taft 2007). …”

Section: Discussionmentioning

confidence: 99%

“…The numbers of GCs in the hilus were studied at three ages: 16, 30 and 60 days after birth (postnatal day or PND16, 30, and 60). These ages were selected because they reflect three developmental stages: 1) a time during development when the DG cell layers have become well defined, but the DG is still not mature (PND16), 2) a time when most aspects of DG circuitry have matured but there is still a high proliferation rate (PND30; Bayer 1982; Rao et al 2006; Cushman et al 2012; Ho et al 2012) and 3) shortly after puberty when animals are reproductively mature and therefore adults (PND60; Pritchett and Taft 2007). …”

Section: Introductionmentioning

confidence: 99%

Hilar granule cells of the mouse dentate gyrus: effects of age, septotemporal location, strain, and selective deletion of the proapoptotic gene BAX

Bermudez-Hernandez

Moretto

et al. 2017

Brain Struct Funct

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The dentate gyrus (DG) principal cells are glutamatergic granule cells (GCs) and they are located in a compact cell layer. However, GCs are also present in the adjacent hilar region, but have been described in only a few studies. Therefore we used the transcription factor prospero homeobox 1 (Prox1) to quantify GCs at postnatal day (PND) 16, 30 and 60 in a common mouse strain, C57BL/6J mice. At PND16, there was a large population of Prox1-immunoreactive (ir) hilar cells, with more in the septal than temporal hippocampus. At PND30 and 60, the size of the hilar Prox1-ir cell population was reduced. Similar numbers of hilar Prox1-expressing cells were observed in PND30 and 60 Swiss Webster mice. Prox1 is usually considered to be a marker of postmitotic GCs. However, many Prox1-ir hilar cells, especially at PND16, were not double-labeled with NeuN, a marker typically found in mature neurons. Most hilar Prox1-positive cells at PND16 co-expressed doublecortin (DCX) and calretinin, markers of immature GCs. Double-labeling with a marker of actively dividing cells, Ki67, was not detected. These results suggest that, surprisingly, a large population of cells in the hilus at PND16 are immature GCs (Type 2b and Type 3 cells). We also asked whether hilar Prox1-ir cell numbers are modifiable. To examine this issue we conditionally deleted the proapoptotic gene BAX in Nestin-expressing cellss at a time when there are numerous immature GCs in the hilus, PND2-8. When these mice were examined at PND60, the numbers of Prox1-ir hilar cells were significantly increased compared to control mice. However, deletion of BAX did not appear to change the proportion that co-expressed NeuN, suggesting that the size of the hilar Prox1-expressing population is modifiable. However, deleting BAX, a major developmental disruption, does not appear to change the proportion that ultimately become neurons.

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“…[56]. However, among inbred strains there is variability in many traits including response to superovulation, developmental capacity of embryos in vivo and in vitro and in the efficiency with which embryos can be used to produce transgenic mice [57][58][59][60].…”

Section: The Mouse As a Model For The Mousementioning

confidence: 99%

Virtues and limitations of the preimplantation mouse embryo as a model system

Taft

2008

Theriogenology

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The mouse is the most widely used model of preimplantation embryo development, but is it a good model? Its small size, prolificacy and ease of handling make the mouse a relatively low cost, readily available and attractive alternative when embryos from other species are difficult or expensive to obtain. However, the real power of the mouse as a model lies in mouse genetics. The development of inbred mouse strains facilitated gene discovery as well as our understanding of gene function and regulation while the development of tools to introduce precise genetic modifications uniquely positioned the mouse as a powerful model system for uncovering gene function. However, all models have limitations; the small size of the mouse limits tissue availability and manipulations that can be performed and differences in physiology among species may make it inappropriate to extrapolate from the mouse to other species. Thus, rather than extrapolating directly from the mouse to other species, it may be more useful to use the mouse as a model system for developing and refining hypotheses to be tested directly in species of interest. In this brief review, the value of the preimplantation mouse embryo as a model is considered, both as a model for other species and as a model for the mouse, as understanding the virtues and limitations of the mouse as a model system is essential to its appropriate use.

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Reproductive Biology of the Laboratory Mouse

Cited by 24 publications

References 273 publications

Genetic and Maternal Effects on Offspring Mortality in Mice

Genetic and Maternal Effects on Offspring Mortality in Mice

Hilar granule cells of the mouse dentate gyrus: effects of age, septotemporal location, strain, and selective deletion of the proapoptotic gene BAX

Virtues and limitations of the preimplantation mouse embryo as a model system

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