Apterous Regulates the Formation of Stable Myotendinous Junctions in the Drosophila Embryo
Authors: Basya Buchbinder 1; Xyomara Wutoh-Hughes 1; Mary Baylies 3,4; Krista Dobi 1, 2
Affiliations: 1) Department of Natural Sciences, Bernard M. Baruch College, City University of New York, New York, NY; 2) PhD Program in Biology, The Graduate Center, City University of New York, New York, NY; 3) Developmental Biology Program, Sloan Kettering Institute, Memorial Sloan Kettering Cancer Center, New York, NY; 4) Biochemistry, Cell & Developmental Biology, and Molecular Biology (BCMB) Program, Weill Cornell Graduate School of Medical Sciences, New York, NY
Keywords: j. muscle; a. cytoskeleton
Skeletal muscles are required for locomotion such as walking, grasping, blinking and chewing. To accomplish these movements, muscles must form secure tendon attachments that can withstand the force of contraction. It is vital that strong attachments form between the right pairs muscle and tendons during development. These myotendinous junctions link transmembrane Integrin proteins to the cytoskeleton and sarcomere. In the Drosophila embryo thirty distinct muscles make up each abdominal hemisegment. While certain muscle subsets are known to have specific guidance cues (for example, ventrolateral muscles use the protein Kon-tiki), a gap in our knowledge exists about how the lateral transverse muscles regulate where and how their attachments are formed. We have identified the transcription factor Apterous as important for the formation of robust muscle attachments. Apterous is expressed in and required for the appropriate patterning of all four lateral transverse muscles in each abdominal hemisegment. We find that embryos with gain or loss of Apterous function display attachment defects, including missing or incorrect attachments. Misexpression of Apterous leads to severe disruptions to the muscle pattern, including an increase in lateral transverse-like muscle morphologies. Moreover, using time-lapse confocal imaging, we show that misexpression of apterous in the somatic musculature leads to loss of muscle attachment upon the onset of contractions, resulting in an inability to hatch and embryonic death. We demonstrate that overexpression of apterous leads to loss of both beta-PS Integrin and alpha-PS2 Integrin from myotendinous junctions. Our work establishes a clear function for apterous in the regulation of muscle attachment, linking changes in gene expression to alterations in muscle morphology.