Distinct signal/response mechanisms regulate pax1 and QmyoD activation in sclerotomal and myotomal lineages of quail somites.
Pax1 and QmyoD are early sclerotome and myotome-specific genes that are activated in epithelial somites of quail embryos in response to axial notochord/neural tube signals. In situ hybridization experiments reveal that the developmental kinetics of activation of pax1 and QmyoD differ greatly, suggesting that myotome and sclerotome specification are controlled by distinct developmental mechanisms. pax1 activation always occurs in somite IV throughout development, indicating that pax1 regulation is tightly coordinated with early steps in somite maturation. In contrast, QmyoD is delayed and does not occur until embryos have 12-14 somites. At this time, QmyoD is the first of the myogenic regulatory factor (MRF) genes to be activated in preexisting somites in a rapid, anterior to posterior progression until the 22 somite stage, after which time QmyoD is activated in somite I immediately following somite formation. Experiments involving transplantation of newly formed somites to ectopic sites along the anterior to posterior embryonic axis were performed to distinguish the contributions of axial signals and somite response pathways to the developmental regulation of pax1 and QmyoD. These studies show that pax1 activation is regulated by somite formation and maturation, not by the availability of axial signals, which are expressed prior to somite formation. In contrast, the delayed activation of QmyoD is controlled by developmental regulation of the production of axial signals as well as by the competence of somites to respond to these signals. These somite transplantation studies, therefore, provide a basis for understanding the different developmental kinetics of activation of pax1 and QmyoD during sclerotome and myotome specification, and suggest specific molecular models for the developmental regulation of myotome and sclerotome formation in somites through distinct signal/response pathways.
Borycki
A G
AG
Department of Cell and Developmental Biology, University of Pennsylvania School of Medicine, Philadelphia 19104-6058, USA.
Strunk
K E
KE
Savary
R
R
Emerson
C P
CP
D000199:Actins / Q000096:biosynthesis; D000818:Animals; D019070:Cell Lineage; D004268:DNA-Binding Proteins / Q000096:biosynthesis* / Q000235:genetics; D004625:Embryo, Nonmammalian / Q000378:metabolism*; D018507:Gene Expression Regulation, Developmental; D017403:In Situ Hybridization; D017570:MyoD Protein / Q000096:biosynthesis* / Q000235:genetics; D018006:Myogenic Regulatory Factors / Q000096:biosynthesis; D051761:Paired Box Transcription Factors; D011784:Quail / Q000196:embryology*; D015398:Signal Transduction / Q000502:physiology*; D019170:Somites / Q000166:cytology / Q000378:metabolism*; D014157:Transcription Factors / Q000096:biosynthesis* / Q000235:genetics
D000199:Actins; D004268:DNA-Binding Proteins; D017570:MyoD Protein; D018006:Myogenic Regulatory Factors; D051761:Paired Box Transcription Factors; D014157:Transcription Factors; C070835:PAX1 transcription factor