Sterility and Mutants - Genetic Sex Differentiation in Fish - page 149

al. (2010) have generated transgenic zebrafi sh, in which the eGFP: Ntr is
expressed under the control of the spermatocyte specifi c Asp, old and sam
promoters. The transgenic females are fertile; the males have small testes
that are virtually devoid of germ cells and suffer sterility but otherwise
appear normal. Hence the zebrafi sh transgenic line shows a perfect testis
specifi city of inducible male sterility. Hsu et al. (2010) claim that their
'infertile breeding technology' has practical application in controlling
undesired genetically modifi ed fi sh, and meets the standards of biological
and environmental safety.
Whereas the earlier described screens of fi shes have concentrated
on early developmental mutations, the study of Bauer and Goetz (2001)
demonstrates that the mutagenesis can be used to understand the process
of gonadal differentiation and gametogenesis in adults. A mutagenesis
screen has been made on adult zebrafi sh subjected to N-ethyl-nitrosourea
(ENU) as a mutagen and a F 2 crossing scheme has also been used to generate
F 3 homozygous mutants. From a screening of 125 mutagenized genomes
generated in 81 families, 11 mutants, that produce visible phenotypes
in only one sex per family, have been identifi ed. The males suffer three
mutations alone but the females as many as eight. These mutations alter
spermatogenesis with the formation of spermatogonia or spermatocytes
alone and different aspects of ovarian histology. The most interesting
observation made by Bauer and Goetz (2001) is that in these males, the
body size may not affect testis development (cf Loukovitis et al., 2011) but
the ovarian development may directly be linked to body size.
The observations of Feistma et al. (2007) show that thanks to mismatch
repair genes, multiple solutions are present for problems of meiotic crossover/
segregation diffi culties. Male Mlh1 mutant zebrafi sh are sterile and display
an arrest in spermatogenesis at metaphase 1 (Fig. 60), resulting in increased
testis weight due the accumulation of prophase 1 spermatocytes and other
cytological problems including increased apoptosis. Contrastingly, females
are fully fertile but their progeny shows high incidence of malformations
(Fig. 61) and suffers mortality within the fi rst few days of development. SNP
based chromosome analysis revealed that missegregration of chromosomes
at meiosis 1 causes aneuploidy. However a small percentage of surviving
progenies are triploids consisting of both two sets of maternal chromosomes
and one set of paternal chromosomes. The adult triploid males have low
fertility, due to synapsis problems or remain sterile. The frequency triploid
progeny of Mlh1 mutant females is much higher than that expected from
random chromosome segregation. Hence there is a way, though narrow
one, for the Mlh1 mutants to escape into triploids and survive.