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Apoptosis of epaxial myotome in Danforth's short-tail (Sd) mice in somites that form following notochord degeneration.
Dev Biol. 1998 Nov 15; 203(2):276-89.DB

Abstract

Danforth's short-tail (Sd) mouse is a semidominant mutation that prevents completion of notochord development. In homozygous mutant mice, the notochord completely degenerates at embryonic day 9.5 (E9. 5), whereas the neural tube and somites continue to form, permitting analysis of somite development in the absence of inductive signals from the notochord and floor plate. In the somites formed after notochord degeneration, Myf5 expression initiates in a normal temporal sequence, but instead of the normal restriction to the dorsomedial somite, its expression extends into the ventral somite. MyoD, myogenin, and myosin heavy chain are normally expressed in the ventral myotome and there is normal development of hypaxial muscles. In contrast, subsequent to initial Myf5 expression, muscle gene expression was not detected in the dorsal myotome and a high level of apoptosis was observed with significantly decreased formation of epaxial muscles. The apoptosis of epaxial muscle in somites that formed after notochord degeneration is consistent with a role for the notochord in the survival and differentiation of the dorsal myotome.

Authors+Show Affiliations

Division of Molecular Medicine, Fred Hutchinson Cancer Research Center, 1124 Columbia Street, Seattle, Washington, 98104, USA.No affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

9808779

Citation

Asakura, A, and S J. Tapscott. "Apoptosis of Epaxial Myotome in Danforth's Short-tail (Sd) Mice in Somites That Form Following Notochord Degeneration." Developmental Biology, vol. 203, no. 2, 1998, pp. 276-89.
Asakura A, Tapscott SJ. Apoptosis of epaxial myotome in Danforth's short-tail (Sd) mice in somites that form following notochord degeneration. Dev Biol. 1998;203(2):276-89.
Asakura, A., & Tapscott, S. J. (1998). Apoptosis of epaxial myotome in Danforth's short-tail (Sd) mice in somites that form following notochord degeneration. Developmental Biology, 203(2), 276-89.
Asakura A, Tapscott SJ. Apoptosis of Epaxial Myotome in Danforth's Short-tail (Sd) Mice in Somites That Form Following Notochord Degeneration. Dev Biol. 1998 Nov 15;203(2):276-89. PubMed PMID: 9808779.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Apoptosis of epaxial myotome in Danforth's short-tail (Sd) mice in somites that form following notochord degeneration. AU - Asakura,A, AU - Tapscott,S J, PY - 1998/11/11/pubmed PY - 1998/11/11/medline PY - 1998/11/11/entrez SP - 276 EP - 89 JF - Developmental biology JO - Dev Biol VL - 203 IS - 2 N2 - Danforth's short-tail (Sd) mouse is a semidominant mutation that prevents completion of notochord development. In homozygous mutant mice, the notochord completely degenerates at embryonic day 9.5 (E9. 5), whereas the neural tube and somites continue to form, permitting analysis of somite development in the absence of inductive signals from the notochord and floor plate. In the somites formed after notochord degeneration, Myf5 expression initiates in a normal temporal sequence, but instead of the normal restriction to the dorsomedial somite, its expression extends into the ventral somite. MyoD, myogenin, and myosin heavy chain are normally expressed in the ventral myotome and there is normal development of hypaxial muscles. In contrast, subsequent to initial Myf5 expression, muscle gene expression was not detected in the dorsal myotome and a high level of apoptosis was observed with significantly decreased formation of epaxial muscles. The apoptosis of epaxial muscle in somites that formed after notochord degeneration is consistent with a role for the notochord in the survival and differentiation of the dorsal myotome. SN - 0012-1606 UR - https://www.unboundmedicine.com/medline/citation/9808779/Apoptosis_of_epaxial_myotome_in_Danforth's_short_tail__Sd__mice_in_somites_that_form_following_notochord_degeneration_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0012-1606(98)99050-9 DB - PRIME DP - Unbound Medicine ER -