Selection for milk somatic cell count in laboratory mice

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dc.contributor.authorLarson, Ann Michelleen
dc.contributor.committeechairVinson, William E.en
dc.contributor.committeememberPearson, Ronald E.en
dc.contributor.committeememberAkers, Robert Michaelen
dc.contributor.committeememberMcGilliard, Michael L.en
dc.contributor.departmentDairy Scienceen
dc.date.accessioned2014-03-14T21:41:57Zen
dc.date.adate2012-08-01en
dc.date.available2014-03-14T21:41:57Zen
dc.date.issued1988-12-15en
dc.date.rdate2012-08-01en
dc.date.sdate2012-08-01en
dc.description.abstractA bidirectional selection experiment for high and low somatic cell count (SCC) was conducted over 14 generations with two selected lines (high line = HSCC, low line = LSCC) of mice. Seven secondary traits (milk yield, total white blood cell count, percentage of phagocytic cells in blood, endotoxin challenge response, percentage of females littering, number of young born alive, and percentage of young surviving to weaning) were measured to examine correlated responses to selection for SCC. Average response per generation for log2 SCC was small in both selected lines (HSCC = .0678 ±.0341, LSCC = .0384 ± .0390, P > .05). There was little per generation divergence between the selected lines (.0294 ± .0178, P > .05). Genetic and phenotypic selection differentials indicated that selection procedures did select the more extreme individuals for SCC, even though response to selection was poor. Phenotypic correlations among SCC and the seven secondary traits were generally small, and near zero. Correlation coefficients ranged from -.17 to .17. Milk yield was negatively correlated with SCC (-.07, P < .05). The correlation between endotoxin challenge response and SCC was also negative (-.17, P < .05). Components of genetic variance for SCC were estimated to explain the lack of selection response. Covariances between daughter and dam, and among full sibs were negative (-.1180 and -.0362, respectively). Analysis for offspring and maternal components for SCC yielded a negative estimate for the covariance between additive effects for the offspring and maternal components (-.1781). No biological explanation can be offered for its existence. Heritability from this same analysis was .05.en
dc.description.degreeMaster of Scienceen
dc.format.extentix, 85 leavesen
dc.format.mediumBTDen
dc.format.mimetypeapplication/pdfen
dc.identifier.otheretd-08012012-040326en
dc.identifier.sourceurlhttp://scholar.lib.vt.edu/theses/available/etd-08012012-040326/en
dc.identifier.urihttp://hdl.handle.net/10919/44079en
dc.publisherVirginia Techen
dc.relation.haspartLD5655.V855_1988.L372.pdfen
dc.relation.isformatofOCLC# 19609258en
dc.rightsIn Copyrighten
dc.rights.urihttp://rightsstatements.org/vocab/InC/1.0/en
dc.subject.lccLD5655.V855 1988.L372en
dc.subject.lcshMastitisen
dc.subject.lcshMice -- Diseasesen
dc.subject.lcshSomatic cellsen
dc.titleSelection for milk somatic cell count in laboratory miceen
dc.typeThesisen
dc.type.dcmitypeTexten
thesis.degree.disciplineDairy Scienceen
thesis.degree.grantorVirginia Polytechnic Institute and State Universityen
thesis.degree.levelmastersen
thesis.degree.nameMaster of Scienceen

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