scholarly journals Imposex, female sterility and organotin contamination of the prosobranch Nassarius reticulatus from the Portuguese coast

2002 ◽  
Vol 230 ◽  
pp. 127-135 ◽  
Author(s):  
CM Barroso ◽  
MH Moreira ◽  
MJ Bebianno
2008 ◽  
Vol 56 (7) ◽  
pp. 1323-1331 ◽  
Author(s):  
Miléne Rato ◽  
Miguel B. Gaspar ◽  
Shin Takahashi ◽  
Shinichi Yano ◽  
Shinsuke Tanabe ◽  
...  

Genetics ◽  
2000 ◽  
Vol 154 (4) ◽  
pp. 1721-1733
Author(s):  
Daryl S Henderson ◽  
Ulrich K Wiegand ◽  
David G Norman ◽  
David M Glover

Abstract Proliferating cell nuclear antigen (PCNA) functions in DNA replication as a processivity factor for polymerases δ and ε, and in multiple DNA repair processes. We describe two temperature-sensitive lethal alleles (mus209B1 and mus2092735) of the Drosophila PCNA gene that, at temperatures permissive for growth, result in hypersensitivity to DNA-damaging agents, suppression of position-effect variegation, and female sterility in which ovaries are underdeveloped and do not produce eggs. We show by mosaic analysis that the sterility of mus209B1 is partly due to a failure of germ-line cells to proliferate. Strikingly, mus209B1 and mus2092735 interact to restore partial fertility to heteroallelic females, revealing additional roles for PCNA in ovarian development, meiotic recombination, and embryogenesis. We further show that, although mus209B1 and mus2092735 homozygotes are each defective in repair of transposase-induced DNA double-strand breaks in somatic cells, this defect is substantially reversed in the heteroallelic mutant genotype. These novel mutations map to adjacent sites on the three-dimensional structure of PCNA, which was unexpected in the context of this observed interallelic complementation. These mutations, as well as four others we describe, reveal new relationships between the structure and function of PCNA.


Genetics ◽  
2004 ◽  
Vol 166 (2) ◽  
pp. 789-796 ◽  
Author(s):  
Kyoichi Sawamura ◽  
John Roote ◽  
Chung-I Wu ◽  
Masa-Toshi Yamamoto

Abstract Recent genetic analyses of closely related species of Drosophila have indicated that hybrid male sterility is the consequence of highly complex synergistic effects among multiple genes, both conspecific and heterospecific. On the contrary, much evidence suggests the presence of major genes causing hybrid female sterility and inviability in the less-related species, D. melanogaster and D. simulans. Does this contrast reflect the genetic distance between species? Or, generally, is the genetic basis of hybrid male sterility more complex than that of hybrid female sterility and inviability? To clarify this point, the D. simulans introgression of the cytological region 34D-36A to the D. melanogaster genome, which causes recessive male sterility, was dissected by recombination, deficiency, and complementation mapping. The 450-kb region between two genes, Suppressor of Hairless and snail, exhibited a strong effect on the sterility. Males are (semi-)sterile if this region of the introgression is made homozygous or hemizygous. But no genes in the region singly cause the sterility; this region has at least two genes, which in combination result in male sterility. Further, the males are less fertile when heterozygous with a larger introgression, which suggests that dominant modifiers enhance the effects of recessive genes of male sterility. Such an epistatic view, even in the less-related species, suggests that the genetic complexity is special to hybrid male sterility.


Genetics ◽  
1981 ◽  
Vol 98 (3) ◽  
pp. 565-587
Author(s):  
William R Engels

ABSTRACT In its hypermutable state, an unstable singed allele, snw, mutates in the germline to two other alleleic forms at a total frequency usually between 40 and 60%. In its stable state, the mutation rate of snw is essentially zero. Its state depends on an extrachromosomal condition indistinguishable from a property called cytotype previously studied as a component of hybrid dysgenesis. Of the two known systems of hybrid dysgenesis, denoted P-M and I-R, snw hypermutability is determined by the P-M system and appears to be independent of the I-R system. Cytotype, as defined by the control of snw mutability, is self-reproducing in the cytoplasm or nucleoplasm of the germline through at least two generations. However, it is not entirely autonomous, being ultimately determined by the chromosomes after sufficiently many generations of backcrossing. This combination of chromosomal and extrachromosomal transmission agrees well with previous studies on cytotype. Temperature differences have little effect on the mean mutation rates, but they have a pronounced effect on the intrinsic variance among individuals. The latter effect suggests that high temperatures reduce germ-cell survival during the development of dysgenic flies. Chromosomal rearrangements produce no apparent effects on the behavior of snw. Hypermutability is thought to be caused by the excision or other alteration of an inserted genetic element in the snw gene. This element might be a copy of the "P factor," which is though to be a mobile sequence capable of causing female sterility and other dysgenic traits in the P-M system.


Genetics ◽  
1996 ◽  
Vol 143 (1) ◽  
pp. 175-189 ◽  
Author(s):  
Jin-rong Xu ◽  
John F Leslie

Abstract We constructed a recombination-based map of the fungal plant pathogen Gibberella fujikuroi mating population A (asexual stage Fusarium moniliforme). The map is based on the segregation of 142 restriction fragment length polymorphism (RFLP) markers, two auxotrophic genes (arg1, nic1), mating type (matA+ / matA−), female sterility (ste1), spore-killer (Sk), and a gene governing the production of the mycotoxin fumonisin B1 (fum1) among 121 random ascospore progeny from a single cross. We identified 12 linkage groups corresponding to the 12 chromosome-sized DNAs previously observed in contour-clamped homogeneous electric field (CHEF) gels. Linkage groups and chromosomes were correlated via Southern blots between appropriate RFLP markers and the CHEF gels. Eleven of the 12 chromosomes are meiotically stable, but the 12th (and smallest) is subject to deletions in 3% (4/121) of the progeny. Positive chiasma interference occurred on five of the 12 chromosomes, and nine of the 12 chromosomes averaged more than one crossover per chromosome. The average kb/cM ratio in this cross is ~32.


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