2024-03-29T02:07:02Zhttp://digital.csic.es/dspace-oai/requestoai:digital.csic.es:10261/241462021-12-28T16:08:10Zcom_10261_79com_10261_1col_10261_332
http://hdl.handle.net/10261/24146
10.1371/journal.pone.0006960
24382
The Complex Spatio-Temporal Regulation of the Drosophila Myoblast Attractant Gene duf/kirre
Public Library of Science
2009
artículo
Guruharsha, K.G.
Ruiz-Gómez, Mar
Ranganath, H. A.
Siddharthan, Rahul
VijayRaghavan, K.
Drosophila
duf/kirre
2009-09-09
A key early player in the regulation of myoblast fusion is the gene dumbfounded (duf, also known as kirre). Duf must be
expressed, and function, in founder cells (FCs). A fixed number of FCs are chosen from a pool of equivalent myoblasts and
serve to attract fusion-competent myoblasts (FCMs) to fuse with them to form a multinucleate muscle-fibre. The spatial and
temporal regulation of duf expression and function are important and play a deciding role in choice of fibre number,
location and perhaps size. We have used a combination of bioinformatics and functional enhancer deletion approaches to
understand the regulation of duf. By transgenic enhancer-reporter deletion analysis of the duf regulatory region, we found
that several distinct enhancer modules regulate duf expression in specific muscle founders of the embryo and the adult. In
addition to existing bioinformatics tools, we used a new program for analysis of regulatory sequence, PhyloGibbs-MP,
whose development was largely motivated by the requirements of this work. The results complement our deletion analysis
by identifying transcription factors whose predicted binding regions match with our deletion constructs. Experimental
evidence for the relevance of some of these TF binding sites comes from available ChIP-on-chip from the literature, and
from our analysis of localization of myogenic transcription factors with duf enhancer reporter gene expression. Our results
demonstrate the complex regulation in each founder cell of a gene that is expressed in all founder cells. They provide
evidence for transcriptional control—both activation and repression—as an important player in the regulation of myoblast
fusion. The set of enhancer constructs generated will be valuable in identifying novel trans-acting factor-binding sites and
chromatin regulation during myoblast fusion in Drosophila. Our results and the bioinformatics tools developed provide a
basis for the study of the transcriptional regulation of other complex genes.
openAccess
PLoS ONE
4
e6960