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The small heat shock protein Hsp27 has been shown to be involved in a diverse array of cellular processes, including cellular stress response, protein chaperone activity, regulation of cellular glutathione levels, apoptotic signaling, and regulation of actin polymerization and stability. Furthermore, mutation within Hsp27 has been associated with the human congenital neuropathy Charcot-Marie Tooth (CMT) disease. Hsp27 is known to be expressed in developing embryonic tissues; however, little has been done to determine the endogenous requirement for Hsp27 in developing embryos. In this study, we show that depletion of XHSP27 protein results in a failure of cardiac progenitor fusion resulting in cardia bifida. Furthermore, we demonstrate a concomitant disorganization of actin filament organization and defects in myofibril assembly. Moreover, these defects are not associated with alterations in specification or differentiation. We have thus demonstrated a critical requirement for XHSP27 in developing cardiac and skeletal muscle tissues.
FIG. 2. XHsp27 is expressed in
the gastrula, and developing skeletal
and cardiac muscle. Whole
mount in situ hybridization of X.
laevis embryos using an antisense
probe specific for XHsp27 at the
indicated stages. (a) Dorsal is to
the top. (b�i) Anterior is to the left.
(j�m) Transverse sections through
somitic (j, k) and cardiac (l, m)
regions. Dorsal is to the top. b,
body muscle; br, brain; h, heart; j,
jaw muscle, m, myotome; mc,
myocardium.
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