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Plant Cell Advance Online Publication
Published on April 3, 2009; 10.1105/tpc.109.066159


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Received February 10, 2009
Returned for revision March 11, 2009
Accepted March 18, 2009

Controlled Enlargement of the Glycoprotein Vesicle Surrounding a Volvox Embryo Requires the InvB Nucleotide-Sugar Transporter and Is Required for Normal Morphogenesis

Noriko Ueki 1* and Ichiro Nishii 1

1 Nishii Initiative Research Unit, RIKEN Advanced Science Institute, Wako-shi, 351-0198, Japan

* To whom correspondence should be addressed. E-mail: noriko.ueki{at}uni-bielefeld.de.

Here, we report our analysis of a mutant of Volvox carteri, InvB, whose embryos fail to execute inversion, the process in which each Volvox embryo normally turns itself inside-out at the end of embryogenesis, thereby achieving the adult configuration. The invB gene encodes a nucleotide-sugar transporter that exhibits GDP-mannose transport activity when expressed in yeast. In wild-type embryos, the invB transcript is maximally abundant before and during inversion. A mannoside probe (fluorescent concanavalin A) stains the glycoprotein-rich gonidial vesicle (GV) surrounding wild-type embryos much more strongly than it stains the GV surrounding InvB embryos. Direct measurements revealed that throughout embryogenesis the GV surrounding a wild-type embryo increases in size much more than the GV surrounding an InvB embryo does, and the fully cleaved InvB embryo is much more tightly packed within its GV than a wild-type embryo is. To test the hypothesis that the restraint imposed by a smaller than normal GV directly causes the inversion defect in the mutant, we released InvB embryos from their GVs microsurgically. The resulting embryos inverted normally, demonstrating that controlled enlargement of the GV, by a process in which requires the InvB nucleotide-sugar transporter, is essential to provide the embryo sufficient space to complete inversion.




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N. A. Eckardt
A Volvox Inversionless Mutant Highlights the Importance of the Extracellular Matrix in Morphogenesis
PLANT CELL, April 1, 2009; 21(4): 1029 - 1029.
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