Distributive pairing in the grasshopper Chorthippus binotatus

Genome ◽  
1991 ◽  
Vol 34 (1) ◽  
pp. 139-143 ◽  
Author(s):  
M. D. Lopez-Leon ◽  
J. Cabrero ◽  
J. P. M. Camacho

Six males of the grasshopper Chorthippus binotatus were mosaic for the presence of extra (E) chromosomes in the germ line, but lacked them in the somatic cells of gastric caeca. E chromosomes were very similar to the X chromosome in size and meiotic properties (heteropycnosis and autopairing). X and E chromosomes associated frequently at diplotene, but the associations never persisted until metaphase I, which indicated that they were not chiasmate. When one E was present, X and E univalents segregated preferentially to opposite poles. In cells with two E, they formed a bivalent in almost all cells, and decreased the frequency of X–E associations by 20%. These cells showed a high frequency of nondisjunction between the two E chromosomes, such that they segregated independently despite the high persistence of their association at metaphase I. These results are interpreted and discussed in the light of the distributive pairing model.Key words: distributive pairing, X chromosome, E chromosome, Chorthippus, male meiosis.

eLife ◽  
2015 ◽  
Vol 4 ◽  
Author(s):  
Daniel B Cortes ◽  
Karen L McNally ◽  
Paul E Mains ◽  
Francis J McNally

Trisomy, the presence of a third copy of one chromosome, is deleterious and results in inviable or defective progeny if passed through the germ line. Random segregation of an extra chromosome is predicted to result in a high frequency of trisomic offspring from a trisomic parent. Caenorhabditis elegans with trisomy of the X chromosome, however, have far fewer trisomic offspring than expected. We found that the extra X chromosome was preferentially eliminated during anaphase I of female meiosis. We utilized a mutant with a specific defect in pairing of the X chromosome as a model to investigate the apparent bias against univalent inheritance. First, univalents lagged during anaphase I and their movement was biased toward the cortex and future polar body. Second, late-lagging univalents were frequently captured by the ingressing polar body contractile ring. The asymmetry of female meiosis can thus partially correct pre-existing trisomy.


2015 ◽  
Vol 112 (47) ◽  
pp. 14415-14422 ◽  
Author(s):  
Sha Sun ◽  
Bernhard Payer ◽  
Satoshi Namekawa ◽  
Jee Young An ◽  
William Press ◽  
...  

The long noncoding X-inactivation–specific transcript (Xist gene) is responsible for mammalian X-chromosome dosage compensation between the sexes, the process by which one of the two X chromosomes is inactivated in the female soma. Xist is essential for both the random and imprinted forms of X-chromosome inactivation. In the imprinted form, Xist is paternally marked to be expressed in female embryos. To investigate the mechanism of Xist imprinting, we introduce Xist transgenes (Tg) into the male germ line. Although ectopic high-level Xist expression on autosomes can be compatible with viability, transgenic animals demonstrate reduced fitness, subfertility, defective meiotic pairing, and other germ-cell abnormalities. In the progeny, paternal-specific expression is recapitulated by the 200-kb Xist Tg. However, Xist imprinting occurs efficiently only when it is in an unpaired or unpartnered state during male meiosis. When transmitted from a hemizygous father (+/Tg), the Xist Tg demonstrates paternal-specific expression in the early embryo. When transmitted by a homozygous father (Tg/Tg), the Tg fails to show imprinted expression. Thus, Xist imprinting is directed by sequences within a 200-kb X-linked region, and the hemizygous (unpaired) state of the Xist region promotes its imprinting in the male germ line.


Genetics ◽  
1982 ◽  
Vol 100 (2) ◽  
pp. 209-237
Author(s):  
Danielle Thierry-Mieg

ABSTRACT The genetic properties of a pleiotropic mutant mapping at 1.4 ± 0.1 in band 3B3 or its adjacent interbands on the X chromosome are described. The mutation is expressed autonomously in germ line cells, where it is recessive and has antimorphic properties. At 29°, the mutation blocks oocyte differentiation, causing female sterility. At lower temperatures, it disturbs the maternal information in the egg; as a result, the progeny lack germ line cells (grandchildless phenotype) and exhibit defects of the cuticular pattern. The mutation is also expressed in somatic cells through zygotic interactions with neighboring regions, including 3A2, 3A3 (zeste), 3C1-2, 3C4 and 3C6-8 (Notch). We interpret the data by postulating that the expression of sets of dispersed genes might be controlled by the local topology of the chromosome, itself constrained by pairing of dispersed repeated elements. We call the mutation paralog.


Genetics ◽  
1986 ◽  
Vol 112 (2) ◽  
pp. 359-383
Author(s):  
B Charlesworth ◽  
C H Langley

ABSTRACT This paper examines the conditions under which self-regulated rates of transposition can evolve in populations of transposable elements infecting sexually reproducing hosts. Models of the evolution of both cis-acting regulation (transposition immunity) and trans-acting regulation (transposition repression) are analyzed. The potential selective advantage to regulation is assumed to be derived from the deleterious effects of mutations associated with the insertion of newly replicated elements. It is shown that both types of regulation can easily evolve in hosts with low rates of genetic recombination per generation, such as bacteria or bacterial plasmids. Conditions are much more restrictive in organisms with relatively free recombination. In haploids, the main selective force promoting regulation is the induction of lethal or sterile mutations by transposition; in diploids, a sufficiently high frequency of dominant lethal or sterile mutations associated with transpositions is required. Data from Drosophila and maize suggest that this requirement can sometimes be met. Coupling of regulatory effects across different families of elements would also aid the evolution of regulation. The selective advantages of restricting transposition to the germ line and of excising elements from somatic cells are discussed.


Genetics ◽  
1995 ◽  
Vol 139 (2) ◽  
pp. 697-711 ◽  
Author(s):  
N Prud'homme ◽  
M Gans ◽  
M Masson ◽  
C Terzian ◽  
A Bucheton

Abstract Gypsy is an endogenous retrovirus of Drosophila melanogaster. It is stable and does not transpose with detectable frequencies in most Drosophila strains. However, we have characterized unstable strains, known as MG, in which it transposes at high frequency. These stocks contain more copies of gypsy than usual stocks. Transposition results in mutations in several genes such as ovo and cut. They are stable and are due to gypsy insertions. Integrations into the ovoD1 female sterile-dominant mutation result in a null allele of the gene and occurrence of fertile females. This phenomenon, known as the ovoD1 reversion assay, can be used to quantitate gypsy activity. We have shown that the properties of MG strains result from mutation of a host gene that we called flamenco (flam). It has a strict maternal effect on gypsy mobilization: transposition occurs at high frequency only in the germ line of the progeny of females homozygous for mutations of the gene. It is located at position 65.9 (20A1-3) on the X chromosome. The mutant allele present in MG strains is essentially recessive. Flamenco seems to control the infective properties of gypsy.


Development ◽  
1990 ◽  
Vol 108 (Supplement) ◽  
pp. 63-72 ◽  
Author(s):  
Bruce M. Cattanach ◽  
Colin V. Beechey

Mouse genetic studies using Robertsonian and reciprocal translations have shown that certain autosomal regions of loci are subject to a parental germ line imprint, which renders maternal and paternal copies functionally inequivalent in the embryo or later stages of development. Duplication of maternal or paternal copies with corresponding paternal/maternal deficiencies in chromosomally balanced zygotes causes various effects. These range from early embryonic lethalities through to mid-fetal and neonatal lethalities, and in some instances viable young with phenotypic effects are obtained. Eight to nine chromosomal regions that give such imprinting effects have been identified. Six to seven of these regions are located in only three chromosomes (2, 7 and 17). The two other regions are located in chromosomes 6 and 11. Maternal and paternal disomies for each of four other chromosomes (1, 5, 9 and 14) have been recovered with different frequencies, but the possibility that this may be due to imprinting has yet to be supported by follow-up studies on regions of the chromosomes concerned. No clear evidence of genetic-background modifications of the imprinting process have been observed in these mouse genetic experiments. The mammalian X chromosome is also subject to imprinting, as demonstrated by the non-random, paternal X-inactivation in female mouse extra-embryonic tissues and in the somatic cells of marsupial females. There is also the opposite bias towards inactivation of the maternal X in the somatic cells of female mice. On the basis that both X-chromosome inactivation and autosomal chromosome imprinting may be concerned with gene regulation, it is suggested that evidence from X-chromosome inactivation studies may help to elucidate factors underlying the imprinting of autosomes. The relevant aspects of X-inactivation are summarized.


Genome ◽  
1989 ◽  
Vol 32 (6) ◽  
pp. 941-945 ◽  
Author(s):  
Wolfgang Staiber

The pairing behavior of the germ line limited chromosomes of Acricotopus lucidus was investigated in male meiosis using G-banding. Each of the nine different types of limited chromosomes can be absent or can be present in metaphase I with two or four homologous chromosomes, one type even with up to 10. Usually the homologues form bivalents, but frequently quadrivalents and also hexavalents consisting of the same chromosome type were observed. In some cases multivalents composed of different limited chromosomes occurred. This resulted probably from pairing and crossing-over between hom(oe)ologous segments in otherwise nonhomologous chromosomes. The observations are discussed in relation to origin and diversity of the germ line limited chromosomes.Key words: germ line limited chromosomes, multivalent formation, male meiosis, Acricotopus lucidus.


Genome ◽  
1989 ◽  
Vol 31 (2) ◽  
pp. 625-637 ◽  
Author(s):  
Jonathan Hodgkin ◽  
Andrew D. Chisholm ◽  
Michael M. Shen

Sex determination in Caenorhabditis elegans involves a cascade of major regulatory genes connecting the primary sex determining signal, X chromosome dosage, to key switch genes, which in turn direct development along either male or female pathways. Animals with one X chromosome (XO) are male, while animals with two X chromosomes (XX) are hermaphrodite: hermaphrodite development occurs because the action of the regulatory genes is modified in the germ line so that both sperm and oocytes are made inside a completely female soma. The regulatory genes are being examined by both genetic and molecular means. We discuss how these major genes, in particular the last switch gene in the cascade, tra-1, might regulate the many different sex-specific events that occur during the development of the hermaphrodite and of the male.Key words: nematode, Caenorhabditis elegans, sex determination, sexual differentiation, cell lineage analysis.


2006 ◽  
Vol 44 ◽  
pp. S240-S241
Author(s):  
D. Roulot ◽  
V. Malan ◽  
V. Bourcier ◽  
B. Benzacken ◽  
M. Ziol ◽  
...  

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