TY - JOUR
T1 - Loss-of-function mutations reveal that the Drosophila nautilus gene is not essential for embryonic myogenesis or viability
AU - Balagopalan, Lakshmi
AU - Keller, Cheryl A.
AU - Abmayr, Susan M.
N1 - Funding Information:
We thank Drs. T. Karr and D. Kiehart for the generous gift of antibodies, Dr. C. Gay for the use of the confocal microscope, and Dr. E. Siegfried for advice on the generation of germline clones. We thank Brian Galletta for critical reading of the manuscript. This work was supported by grants from the National Science Foundation and National Institutes of Health (to S.M.A.).
PY - 2001/3/15
Y1 - 2001/3/15
N2 - nautilus (nau), the single Drosophila member of the bHLH-containing myogenic regulatory family of genes, is expressed in a subset of muscle precursors and differentiated fibers. It is capable of inducing muscle-specific transcription as well as myogenic transformation, and plays a role in the differentiation of a subset of muscle precursors into mature muscle fibers. In previous studies, the nau zygotic loss-of-function phenotype was determined using genetic deficiencies in which the gene is deleted. We note that this genetic loss-of-function phenotype differs from the loss-of-function phenotype determined using RNA interference (L. Misquitta and B. M. Paterson, 1999, Proc. Natl. Acad. Sci. USA 96, 1451-1456). The present study re-examines this loss-of-function phenotype using EMS-induced mutations that specifically alter the nau gene, and extends the genetic analysis to include the loss of both maternal and zygotic nau function. In brief, embryos lacking nau both maternally and zygotically are missing a distinct subset of muscle fibers, consistent with its apparent expression in a subset of muscle fibers. The muscle loss is tolerated, however, such that the loss of nau both maternally and zygotically does not result in lethality at any stage of development.
AB - nautilus (nau), the single Drosophila member of the bHLH-containing myogenic regulatory family of genes, is expressed in a subset of muscle precursors and differentiated fibers. It is capable of inducing muscle-specific transcription as well as myogenic transformation, and plays a role in the differentiation of a subset of muscle precursors into mature muscle fibers. In previous studies, the nau zygotic loss-of-function phenotype was determined using genetic deficiencies in which the gene is deleted. We note that this genetic loss-of-function phenotype differs from the loss-of-function phenotype determined using RNA interference (L. Misquitta and B. M. Paterson, 1999, Proc. Natl. Acad. Sci. USA 96, 1451-1456). The present study re-examines this loss-of-function phenotype using EMS-induced mutations that specifically alter the nau gene, and extends the genetic analysis to include the loss of both maternal and zygotic nau function. In brief, embryos lacking nau both maternally and zygotically are missing a distinct subset of muscle fibers, consistent with its apparent expression in a subset of muscle fibers. The muscle loss is tolerated, however, such that the loss of nau both maternally and zygotically does not result in lethality at any stage of development.
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U2 - 10.1006/dbio.2001.0162
DO - 10.1006/dbio.2001.0162
M3 - Article
C2 - 11237466
AN - SCOPUS:0035869587
SN - 0012-1606
VL - 231
SP - 374
EP - 382
JO - Developmental biology
JF - Developmental biology
IS - 2
ER -