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Kirchstein National Institutional Research Service Award","award":["T32-MH070343"],"award-info":[{"award-number":["T32-MH070343"]}]},{"name":"NIH","award":["1R01MH094607-01A1"],"award-info":[{"award-number":["1R01MH094607-01A1"]}]},{"name":"NSF","award":["IOS_0951019"],"award-info":[{"award-number":["IOS_0951019"]}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["eneuro"],"published-print":{"date-parts":[[2016,7]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>Defects in axonal transport are seen in motoneuronal diseases, but how that impairment comes about is not well understood. In spinal bulbar muscular atrophy (SBMA), a disorder linked to a CAG\/polyglutamine repeat expansion in the androgen receptor (<jats:italic>AR<\/jats:italic>) gene, the disease-causing AR disrupts axonal transport by acting in both a cell-autonomous fashion in the motoneurons themselves, and in a non-cell-autonomous fashion in muscle. The non-cell-autonomous mechanism is suggested by data from a unique \u201cmyogenic\u201d transgenic (TG) mouse model in which an AR transgene expressed exclusively in skeletal muscle fibers triggers an androgen-dependent SBMA phenotype, including defects in retrograde transport. However, motoneurons in this TG model retain the endogenous<jats:italic>AR<\/jats:italic>gene, leaving open the possibility that impairments in transport in this model also depend on ARs in the motoneurons themselves. To test whether non-cell-autonomous mechanisms alone can perturb retrograde transport, we generated male TG mice in which the endogenous<jats:italic>AR<\/jats:italic>allele has the testicular feminization mutation (<jats:italic>Tfm<\/jats:italic>) and, consequently, is nonfunctional. Males carrying the<jats:italic>Tfm<\/jats:italic>allele alone show no deficits in motor function or axonal transport, with or without testosterone treatment. However, when Tfm males carrying the myogenic transgene (Tfm\/TG) are treated with testosterone, they develop impaired motor function and defects in retrograde transport, having fewer retrogradely labeled motoneurons and deficits in endosomal flux based on time-lapse video microscopy of living axons. These findings demonstrate that non-cell-autonomous disease mechanisms originating in muscle are sufficient to induce defects in retrograde transport in motoneurons.<\/jats:p>","DOI":"10.1523\/eneuro.0062-16.2016","type":"journal-article","created":{"date-parts":[[2016,7,22]],"date-time":"2016-07-22T00:39:44Z","timestamp":1469147984000},"page":"ENEURO.0062-16.2016","source":"Crossref","is-referenced-by-count":6,"title":["Non-Cell-Autonomous Regulation of Retrograde Motoneuronal Axonal Transport in an SBMA Mouse Model"],"prefix":"10.1523","volume":"3","author":[{"given":"Katherine","family":"Halievski","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Michael Q.","family":"Kemp","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"S. 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