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Paraspinal muscular defects in Lfng segmentation mutant mice
Author(s) -
Smith Heather F,
Kusumi Kenro,
Rawls Alan,
WilsonRawls Jeanne,
Fisher Rebecca
Publication year - 2009
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.23.1_supplement.825.7
Subject(s) - notch signaling pathway , mutant , anatomy , biology , pathology , gene , medicine , genetics
Mutations in several regulatory genes along the Notch signaling pathway, including Lfng , are associated with vertebral defects and segmentation disorders. However, the role of these genes in regulating myogenic morphology is unknown. The objective of this study was to assess the role of Lfng in determining the morphology of paraspinal musculature. Nine mice that were homozygous null for Lfng and nine wild‐type specimens were dissected and their paraspinal musculature analyzed. Four Lfng null specimens exhibited variation in the iliocostalis muscle, ranging from unilateral reduction to complete bilateral absence. For multifidus, eight Lfng null specimens exhibited variation, including unilateral and bilateral cranial shifts, caudal and cranial reductions, elongations, and one bilateral absence. A χ 2 test revealed a statistically significant difference between the Lfng mutant specimens and wild‐types in the frequency of defects in the iliocostalis and multifidus. These results will be compared to similar findings from Dll3 mutants. The results support the hypothesis that genes in the Notch signaling pathway, Lfng in particular, may influence paraspinal muscular development, although with an incomplete penetrance. These findings have implications for studies of muscular involvement in idiopathic scoliosis and segmentation disorders. This research was partly supported by NIH RO1 AR050687 (KK). Grant Funding Source University of Arizona