Localization of two new X‐linked quantitative trait loci controlling corpus callosum size in the mouse

Kusek, G. K.; Wahłsten, Douglas; Herron, Bruce J.; Bolivar, Valerie J.; Flaherty, Lorraine

doi:10.1111/j.1601-183x.2006.00264.x

Cited by 36 publications

(26 citation statements)

References 18 publications

(24 reference statements)

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“…The cross of 129 and BTBR showed a maternal effect, where mice with a BTBR mother and 129 father had substantially more abnormalities than those with a 129 mother and BTBR father. This pattern supports an earlier finding of an X-linked gene in BTBR that contributes to corpus callosum defects (Kusek et al , 2007). The 129 x BTBR cross was less severely affected than strain 129, whereas the BTBR x 129 cross was more severely abnormal than strain 129.…”

Section: Resultssupporting

confidence: 91%

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Hippocampal commissure defects in crosses of four inbred mouse strains with absent corpus callosum

Bohlen¹,

Bailoo²,

Jordan³

et al. 2012

Genes Brain and Behavior

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It is known that four common inbred mouse strains show defects of the forebrain commissures. The BALB/cJ strain has a low frequency of abnormally small corpus callosum, while the 129 strains have many animals with deficient corpus callosum. The I/LnJ and BTBR T+ tf/J strains never have a corpus callosum, while half of I/LnJ and almost all BTBR show severely reduced size of the hippocampal commissure. Certain of the F1 hybrid crosses among these strains are known to be less severely abnormal than the inbred parents, suggesting the parent strains have different genetic causes of commissure defects. In this study, all hybrid crosses among the four strains were investigated. The BTBR x I/Ln hybrid expressed almost no defects of the hippocampal commissure, unlike its inbred parent strains. Numerous 3-way crosses among the four strains yielded many mice with no corpus callosum and severely reduced hippocampal commissure, which shows that the phenotypic defect can result from several different combinations of genetic alleles. The F2 and F3 hybrid crosses of BTBR and I/LnJ had almost 100% absence of the corpus callosum but about 50% frequency of deficient hippocampal commissure. The 4-way hybrid cross among all four abnormal strains involved highly fertile parents and yielded a very wide phenotypic range of defects from almost no hippocampal commissure to totally normal forebrain commissures. The F2 and F3 crosses as well as the 4-way cross provide excellent material for studies of genetic linkage and behavioral consequences of commissure defects.

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Section: Resultssupporting

confidence: 91%

“…The crosses of BTBR x 129 show a striking reciprocal difference that may arise from an X-linked gene. The same pattern of results was apparent in crosses of BTBR and BALB/cByJ in a previous study (Kusek et al , 2007). The present data for reciprocals of BALB x BTBR (Fig.…”

Section: Discussionsupporting

confidence: 84%

Hippocampal commissure defects in crosses of four inbred mouse strains with absent corpus callosum

Bohlen¹,

Bailoo²,

Jordan³

et al. 2012

Genes Brain and Behavior

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“…Since a number of studies have reported corpus callosum deficits in autistics [11,15,28,54], this corpus callosum deficit in the BTBR strain makes it even more fascinating for further study as a possible mouse model of autism. We have recently mapped the corpus callosum deficiency seen in the BTBR mouse to two quantitative trait loci on the X Chromosome [32]. It is not yet known whether the genes on the X Chromosome that underlie these loci are related to autism, however, ongoing research in our laboratory is addressing that issue.…”

Section: Discussionmentioning

confidence: 99%

Assessing autism-like behavior in mice: Variations in social interactions among inbred strains

Bolivar

Walters

Phoenix

2007

Behavioural Brain Research

246

227

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Autism is a pervasive developmental disorder, with characteristics including impairments in reciprocal social interaction, impaired communication, and repetitive/stereotyped behaviors. Despite decades of research, the etiology of autism remains elusive. Thus, it is important that we pursue all avenues, in attempting to understand this complicated disorder. One such avenue is the development of animal models. While autism may be uniquely human, there are behavioral characteristics of the disorder that can be established in animal models. Evidence supports a genetic component for this disorder, and over the past few decades the mouse has been a highly valuable tool for the elucidation of pathways involved in many human disorders (e.g., Huntington's disease). As a first step toward establishing a mouse model of autism, we studied same-sex social behavior in a number of inbred mouse strains. In Study 1, we examined intra-strain social behavior of male pairs after one mouse had 15 minutes prior exposure to the testing chamber. In Study 2, we evaluated intra-strain and interstrain social behavior when both mice were naive to the testing chamber. The amount and type of social behavior seen differed between these studies, but overall there were general inbred strain differences in social behavior. Some strains were highly social (e.g., FVB/NJ, while others displayed low levels of social behavior (e.g., A/J, BTBR T+ tf/J). These strains may be useful in future genetic studies to determine specific genes involved in mouse social behavior, the findings of which should in turn help us to determine some of the genes involved in human social behavior and its disorders (e.g., autism).

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“…The recent return of BTBR neuroanatomy to autism-related research focus was fueled by the development and popularization of neuroimaging techniques allowing for a more systematic overview of brain morphology aberrations. Until 2013 most information about aberrant brain connectivity in BTBR mice, including the striking complete agenesis of corpus callosum (aCC) and reduction in the hippocampal commissure, came from postmortem histological assessments (Bohlen et al 2012, Jones-Davis et al 2013, Kusek et al 2007, Wahlsten et al 2003). Similar, changes in the shape and localization of many brain structures, including the hippocampus and amygdala (Mercier et al 2012), and the formation of Probst bundles were recently confirmed using these neuroimaging techniques (Dodero et al 2013, Ellegood et al 2013, Fenlon et al 2015, Sforazzini et al 2016, Yang et al 2009).…”

Section: Neuroanatomy Of the Btbr Mouse: Impaired Axon Guidance Anmentioning

confidence: 99%

The BTBR mouse model of idiopathic autism – Current view on mechanisms

Meyza

Blanchard

2017

Neuroscience & Biobehavioral Reviews

136

109

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Autism spectrum disorder (ASD) is the most commonly diagnosed neurodevelopmental disorder, with current estimates of more than 1% of affected children across nations. The patients form a highly heterogeneous group with only the behavioral phenotype in common. The genetic heterogeneity is reflected in a plethora of animal models representing multiple mutations found in families of affected children. Despite many years of scientific effort, for the majority of cases the genetic cause remains elusive. It is therefore crucial to include well-validated models of idiopathic autism in studies searching for potential therapeutic agents. One of these models is the BTBR T+Itpr3tf/J mouse. The current review summarizes data gathered in recent research on potential molecular mechanisms responsible for the autism-like behavioral phenotype of this strain.

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Localization of two new X‐linked quantitative trait loci controlling corpus callosum size in the mouse

Cited by 36 publications

References 18 publications

Hippocampal commissure defects in crosses of four inbred mouse strains with absent corpus callosum

Hippocampal commissure defects in crosses of four inbred mouse strains with absent corpus callosum

Assessing autism-like behavior in mice: Variations in social interactions among inbred strains

The BTBR mouse model of idiopathic autism – Current view on mechanisms

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