recombination or repair functions. The timing of treatment was also critical and the hypermutability ap-
peared only at two times: a few hours before cleavage began in the gonidial cells and then shortly after
the asymmetric cleavage. The hypermutability of the locus is suggested to be a consequence of DNA re-
arrangement: to ensure that the regAgene cannot be expressed in gonidia, it is proposed to be inactivated
by an actual physical rearrangement of the gene itself. The gene is inactivated in pregonidial cells so that
they can express the genes for reproductive function, then reactivated in mature gonidia prior to the first
cleavage as one-celled embryos [21].
C. Sexual Life Cycle and Mutants
A good description of the sexual cycle in Volvoxremained elusive until Darden [22] finally determined
the conditions for its sexual propagation in culture. The cycle is summarized in Figure 3. During asexual
development, males and females are morphologically indistinguishable from one another. After exposure
to the exceedingly potent sexual inducer (active at concentrations lower than 10^16 M), however, both
sexes undergo one more round of asexual cell division and then initiate gamete formation. For female de-
velopment, the gonidia divide symmetrically up to the 64-cell stage, and then up to 48 of the cells divide
asymmetrically and the larger daughter cells form eggs. If fertilization does not occur, the eggs have the
capability of developing into gonidia and continuing development in an asexual manner. After induction,
a male gonidium divides symmetrically up to the 256-cell stage, and then an unequal cleavage of all the
cells produces 256 sperm initials along with somatic cells; the former undergo six or seven further divi-
806 WALLACEFigure 2 Diagrammatic representations of the asexual life cycle of Volvox carteri. Vegetative and repro-
ductive functions are divided between somatic cells and gonidia, respectively. After a number of symmetric di-
visions have occurred, the glsgene acts (at times and places specified by the various mulgenes) to cause a set
of asymmetric cleavage divisions that generate large-small sister cell pairs. In the small somatic initials, the
regAgene is expressed and acts to suppress expression of genes required for gonidial differentiation. These
cells thus become terminally differentiated as somatic cells. In the large gonidial initials, meanwhile, the lag
genes are expressed and the regAgene is inactivated. This leads to repression of the genes required for differ-
entiation of somatic cell features and expression of the genes required for gonidial differentiation. The regA
gene becomes reactivated in mature gonidia some time prior to the first cleavage. (Modified from Ref. 14.)