A comparative assessment of mandible shape in a consomic strain panel of the house mouse (Mus musculus) - implications for epistasis and evolvability of quantitative traits

Boell, Louis; Gregorová, Soňa; Forejt, Jiřı́; Tautz, Diethard

doi:10.1186/1471-2148-11-309

Cited by 19 publications

(37 citation statements)

References 45 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…2; Shao et al 2010;Yazbek et al 2011;DeSantis et al 2013;Kato et al 2014;Winawer et al 2014;Zhu and Matin 2014). The CSSs and congenic strains derived from CSSs have been used to map QTLs and identify causal genetic variants for traits such as body weight, glucose homeostasis, anxiety, hearing loss, bone morphology, blood clotting, liver fibrosis, energy expenditure, seizure susceptibility, among others (Singer et al 2004;Singer 2005;Winawer et al 2007;Gregorová et al 2008;Sa et al 2008;Shao et al 2008;Boell et al 2011;DeSantis et al 2013;Spiezio et al 2014;Street et al 2014). …”

Section: Chromosome Substitution Strains (Csss)mentioning

confidence: 99%

Contrasting genetic architectures in different mouse reference populations used for studying complex traits

Buchner

Nadeau

2015

Genome Res.

View full text Add to dashboard Cite

Quantitative trait loci (QTLs) are being used to study genetic networks, protein functions, and systems properties that underlie phenotypic variation and disease risk in humans, model organisms, agricultural species, and natural populations. The challenges are many, beginning with the seemingly simple tasks of mapping QTLs and identifying their underlying genetic determinants. Various specialized resources have been developed to study complex traits in many model organisms. In the mouse, remarkably different pictures of genetic architectures are emerging. Chromosome Substitution Strains (CSSs) reveal many QTLs, large phenotypic effects, pervasive epistasis, and readily identified genetic variants. In contrast, other resources as well as genome-wide association studies (GWAS) in humans and other species reveal genetic architectures dominated with a relatively modest number of QTLs that have small individual and combined phenotypic effects. These contrasting architectures are the result of intrinsic differences in the study designs underlying different resources. The CSSs examine contextdependent phenotypic effects independently among individual genotypes, whereas with GWAS and other mouse resources, the average effect of each QTL is assessed among many individuals with heterogeneous genetic backgrounds. We argue that variation of genetic architectures among individuals is as important as population averages. Each of these important resources has particular merits and specific applications for these individual and population perspectives. Collectively, these resources together with high-throughput genotyping, sequencing and genetic engineering technologies, and information repositories highlight the power of the mouse for genetic, functional, and systems studies of complex traits and disease models.

show abstract

Section: Chromosome Substitution Strains (Csss)mentioning

confidence: 99%

Contrasting genetic architectures in different mouse reference populations used for studying complex traits

Buchner

Nadeau

2015

Genome Res.

View full text Add to dashboard Cite

show abstract

“…Notably, these studies have provided strong evidence that the quantitative variation for shape is driven by a large number of quantitative trait loci (QTL) (Boell et al 2011; Leamy et al 2008; Navarro and Klingenberg 2007). These QTL act in a pleiotropic manner (Cheverud et al 1997; Ehrich et al 2003) associated with differential dominance, additivity (Ehrich et al 2003), or epistatic buffering (Boell et al 2011).…”

mentioning

confidence: 99%

Exploration of the Genetic Organization of Morphological Modularity on the Mouse Mandible Using a Set of Interspecific Recombinant Congenic Strains Between C57BL/6 and Mice of theMus spretusSpecies

Burgio

Baylac

Heyer

et al. 2012

G3 Genes|Genomes|Genetics

View full text Add to dashboard Cite

Morphological integration and modularity within semi-autonomous modules are essential mechanisms for the evolution of morphological traits. However, the genetic makeup responsible for the control of variational modularity is still relatively unknown. In our study, we tested the hypothesis that the genetic variation for mandible shape clustered into two morphogenetic components: the alveolar group and the ascending ramus. We used the mouse as a model system to investigate genetics determinants of mandible shape. To do this, we used a combination of geometric morphometric tools and a set of 18 interspecific recombinant congenic strains (IRCS) derived from the distantly related species, Mus spretus SEG/Pas and Mus musculus C57BL/6. Quantitative trait loci (QTL) analysis comparing mandible morphometry between the C57BL/6 and the IRCSs identified 42 putative SEG/Pas segments responsible for the genetic variation. The magnitude of the QTL effects was dependent on the proportion of SEG/Pas genome inherited. Using a multivariate correlation coefficient adapted for modularity assessment and a two-block partial least squares analysis to explore the morphological integration, we found that these QTL clustered into two well-integrated morphogenetic groups, corresponding to the ascending ramus and the alveolar region. Together, these results provide evidence that the mouse mandible is subjected to genetic coordination in a modular manner.

show abstract

“…During this early phase, shape was still mainly described by multiple linear measurements and distances and the major problem of capturing the geometry or overall shape of a complex structure persisted. In the 1980s, advances in the development of statistical analytic tools and their combination with outline and landmark data revolutionized the field of geometric morphometrics (Zelditch et al 2012;Rohlf and Marcus 1993;Adams et al 2004;Mitteroecker and Gunz 2009;Adams et al 2013) and sparked studies in facial expression (Adams et al 2013), shape-to-body size correlation (allometry) (Sidlauskas et al 2011), symmetry (Klingenberg et al 2002), quantitative genetics (Klingenberg and Leamy 2001;Boell et al 2011;Pallares et al 2015) and evolutionary-developmental biology (Klingenberg 2010;Salazar-Ciudad and Jernvall 2010) to name but a few.…”

Section: Shape: Description and Quantification Of Complex Structuresmentioning

confidence: 99%

Size and shape—integration of morphometrics, mathematical modelling, developmental and evolutionary biology

Prpic

Posnien

2016

Dev Genes Evol

View full text Add to dashboard Cite

The German philosopher Arthur Schopenhauer (1788-1860) once said: "Any foolish boy can crush a beetle with his foot, but all the professors in the world cannot make a beetle". This quote summarizes the limited knowledge in the midnineteenth century about the mechanisms that generate a new individual. But, it still reflects our limited knowledge of the genetic control of morphogenesis. Studies in a number of model systems, especially in the fruit fly Drosophila melanogaster, have revealed basic principles of how the body axis, segments or organs like the wing are specified, for example. However, we are still lacking a comprehensive understanding of how organisms and their organs know when to stop growing or how to attain their final shape, which is often species specific or even specific to an individual. The basis of size: cell size and cell numbersIn theory, the size of an organ can mainly be changed in two ways: either by changing the size of the individual cells or by changing the number of cells, and thus, an understanding of size control should be possible by studying the mechanisms of cell growth and cell proliferation.In practice, however, the control of cell number and cell size is more complex. For each process, there are several cellular mechanisms. For instance, cell number can be determined not only by controlling the production of new cells but also by killing cells that were already produced (cell death). Thus, positive and negative regulatory mechanisms of cell growth and cell number complement each other. In addition, there is evidence that the mechanisms that control cell growth and those that control cell number can communicate and influence each other. Diploid and tetraploid salamanders, for instance, develop organs of comparable size although in the tetraploid animals, the cells are much larger. The organs compensate for the bigger cell size by reducing the number of cells (Fankhauser 1952). Similarly, a decrease in cell number in plant mutants is associated with an increase in cell size and vice versa. This compensation ensures that despite alterations during development, functional leaves are formed (Gonzalez et al. 2012). Size control: autonomous vs. non-autonomousIn the early 1920s, Harrison and later also Twitty and Schwind transplanted organ anlagen of salamander legs and eyes from a small species into a large species and vice versa. Intriguingly, the size of the transplanted organs always resembled the size in the source species rather than the new host. Thus, the information about their final size must have resided within the transplanted legs and eyes themselves (Harrison 1924; Communicated by Nico Posnien and Nikola-Michael Prpic

show abstract

A comparative assessment of mandible shape in a consomic strain panel of the house mouse (Mus musculus) - implications for epistasis and evolvability of quantitative traits

Cited by 19 publications

References 45 publications

Contrasting genetic architectures in different mouse reference populations used for studying complex traits

Contrasting genetic architectures in different mouse reference populations used for studying complex traits

Exploration of the Genetic Organization of Morphological Modularity on the Mouse Mandible Using a Set of Interspecific Recombinant Congenic Strains Between C57BL/6 and Mice of theMus spretusSpecies

Size and shape—integration of morphometrics, mathematical modelling, developmental and evolutionary biology

Contact Info

Product

Resources

About