This research shows that myoplasmic crescent material of the ascidian egg has both functional autonomy and functional specificity in establishing the differentiation pathway of muscle lineage cells. The cytoplasmic segregation pattern in eggs of Styela plicata was altered by compression of the embryos during third cleavage. This caused a meridional division instead of the normal equatorial third cleavage; first and second cleavages are meridional. Since eggs of S. plicata have a pronounced yellow myoplasmic crescent, one observes directly that third cleavage under compression resulted in a flat 8-cell stage with four cells containing yellow myoplasm instead of the two myoplasm-containing cells that would be formed by normal equatorial division at third cleavage. If such altered 8-cell-stage embryos were released from compression and kept from undergoing further divisions by continuous treatment with cytochalasin B, some embryos eventually developed histospecific acetylcholinesterase in three and four cells instead of in just the two muscle lineage cells found in cleavage-arrested normal 8-cell stages. The wider myoplasmic distribution effected by altering the division plane at third cleavage apparently caused a change in developmental fate of the extra cells receiving myoplasm. This meridional third cleavage also resulted in a changed nuclear lineage pattern. Two nuclei that would ordinarily be in ectodermal lineage cells after third cleavage were now associated with yellow myoplasm. Acetylcholinesterase development in these cells demonstrates that nuclear lineages are not responsible for muscle acetylcholinesterase development in the ascidian embryo.
A Twist-like bHLH gene is a downstream factor of an endogenous FGF and determines mesenchymal fate in the ascidian embryos
