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B F Chadov

Publications and source records attributed to B F Chadov.

At least 19 recordsLinked to original sources
PubMed2006

[A new stage in the development of genetics and term "epigenetics"].

Genetics requires verification of the notion of gene. In this article, DNA and DNA parts are proposed to be named progenes, while the term gene refers to the informational products produced on DNA. These are RNA genes, protein genes, and DNA genes (transposable elements). The focus of genetics is thus switched from characters of intraspecies difference to characters of intraspecies similarity. Regulatory genes controlling ontogeny (ontogenes) become the main object of research. These genes can be isolated by methods of both reverse and direct genetics. The properties of ontogene mutations, produced by methods of direct genetics, are described. The problematic of epigenetics is related to the expression of ontogenes. The term epigenetics is not correct because of its ambiguity.

Animals↗
PubMed2004

[Genes controlling ontogenesis: morphosis, phenocopies, dimorphs, and other visible expressions of mutant genes].

We studied facultative dominant lethal mutations obtained earlier in Drosophila melanogaster. In some genotypes, these mutations were expressed as lethals, but in other genotypes they lacked this expression. The mutations were maintained in the following cultures: (1) females Muller-5 heterozygous for the mutation; (2) males crossed to attached-X females; and females and males homozygous for the mutation. During culturing, many mutations were found to give rise to phenotypically abnormal progeny. Generally, these abnormalities were morphoses involving various body parts; they were mostly asymmetric and non-heritable. Maternal and paternal effects in the formation of morphoses were observed. In four cases, dimorphic mutations were recorded: a female homozygous for the mutation had mutant phenotype whereas its male counterpart was phenotypically normal. The mutations were recessive with regard to the norm. New phenotypes behaving as mutations with incomplete penetrance arose during culturing. In cultures of mutant homozygotes phenocopies would appear en masse; they would persist for one or two generations and disappear. One wave of phenocopies succeeded another. Visible phenotypes appeared, which further behaved as ordinary recessive mutations. We concluded that these visible manifestations are characteristic for regulatory mutations controlling ontogeny. Their appearance is explained by the activation of new regulatory scenarios caused by blocking standard regulatory pathways.

Animals↗
PubMed2004

[The main effect of chromosomal rearrangement is changing the action of regulatory genes].

Effect of chromosomal rearrangements on the expression of mutations was studied in Drosophila melanogaster regulatory genes. These were facultative dominant lethals and recessive lethals on the X chromosome obtained by the classical Muller-5 method. Chromosomal rearrangements drastically changed the expression of regulatory gene mutations. Rearrangements either caused the lethal effect of mutations or suppressed the already present lethality. The action of rearrangements exhibited the maternal or paternal effect. Irrespective of the presence in the genome of mutations at regulatory genes, a rearrangement acted as a factor decreasing fertility of the organism. The rearrangement effect is identical to the expression of regulatory genes per se. It is concluded that the chromosomal rearrangement affects the examined regulatory genes indirectly through a change in the operation of regulatory genes located within the rearrangement. Thus, rearrangements gain great importance for the definition of the pattern of genome functional activity. Widespread distribution of rearrangements in individual genotypes and their effectivity in the process of speciation are thus explained.

Animals↗
PubMed2004

[From genetics of intraspecific differences to genetics of intraspecific similarity].

Based on the Mendelian approach to heredity, modern genetics describes inheritance of characters belonging to the category of intraspecific difference. The other large category of characters, intraspecific similarity, stays out of investigation. In this review, the genome part responsible for intraspecific similarity is considered as invariant and regulatory. An approach to studying the invariant part of the Drosophila melanogaster genome is formulated and the results of examining this genome part are presented. The expression of mutations at genes in the invariant genome part is different from that of Mendelian genes. We conclude that these genes are present in the genome in multiple copies and they are functionally haploid in the diploid genome. Severe abnormalities of development appearing in the progeny of mutant parents suggest that the mutant genes are genes regulating ontogeny. A hypothesis on an elementary ontogenetic event is advanced and the general scheme of ontogeny is presented. A concept on two types of gene allelism (cis- and trans-allelism) is formulated. This approach opens a possibility for studying genetic material responsible for the formation of intraspecific similarity characters at different taxonomic levels on the basis of crossing individuals of the same species.

Animals↗
PubMed2002

[The "image" of the regulatory gene in experiments with Drosophila].

The mutants referred to as facultative dominant lethals were selected in the progeny of gamma-irradiated Drosophila males. The mutant males were viable and fertile, though their crosses with females of the yellow line yielded no daughters. The mutations obtained differed from the common mutations by (1) extremely varying penetrance of F1 hybrids from crosses with various lines; (2) the uncertain relationships between the mutant and normal alleles; (3) the different expression in somatic and germ cells; (4) the dependence of the expression on the sex of the parent carrying the donor mutations; (5) the mass morphosis formation and (6) the frequent reversal to the norm. These mutations are assigned to the regulatory group and their specific expression (see above) can be helpful in identifying regulatory gene mutations. We assume that the specific expression of the mutations studied is related to specific properties of the regulatory genes. These properties are as follows: (1) only one out of two homologous regulatory genes located on one homolog is in an active state, (2) in the haploid chromosome set the regulatory gene is represented by several alleles (cys-alleles); (3) only one allele ensures the regulatory gene activity.

Alleles↗
PubMed2000

[Generation of Y-chromosome insertions into left arm of chromosome 2 of Drosophila melanogaster].

An experimental procedure describing production of insertions of Y-chromosome material into autosomes of Drosophila is presented. Irradiated Y;2 translocations served as source material. The insertion selection scheme was based on the emergence of additional progeny classes in the case of independent segregation of the detached fragments of the Y chromosome and autosome. A total of seven insertions of Y-chromosome material into the left arm of chromosome 2, specifically in regions 29F, 34A, and 36B, were obtained. All insertions were lethal in the homozygous state and caused crossing-over suppression in the left arm of chromosome 2. In addition, these mutations induced the formation of loops between the chromocenter and the region of insertion, as well as breaks in one or both homologs, which are frequently observed in preparations of polytene chromosomes. The selection scheme suggested can be used to produce insertions in any region of Drosophila melanogaster chromosomes 2 and 3, for which the Y;2 translocations exist.

Animals↗
PubMed2000

[Age-related changes in crossing over in Drosophila resemble the picture of interchromosomal effect of chromosome rearrangement on crossing over].

Crossing over in the left arm of chromosome 2 (2L) was studied in successive broods of Drosophila melanogaster females carrying intact chromosomes (+/+), inversion Muller-5 in the X chromosome (M-5/+), and insertion of the Y-chromosome material into region 34A (Is(2L)/+). The regions net-dp, dp-b, b-pr and pr-cn were examined in 14 two-day-old broods of females +/+ and M-5/+ and in 10 broods of females Is(2L)/+. In all lines, the highest level of crossing over was in the first three broods (eggs laid during the first 6 days of oviposition) and the lowest level in the broods 7-8 (eggs laid at days 14-16). A high rate of crossing over in the first broods of females +/+ and M-5/+ was due to an increment of exchanges in the proximal euchromatin regions (b-pr and pr-cn) and to an increase in the number of tetrads with double exchanges. These changes are similar to a pattern of the interchromosomal effect on crossing over (IEC) in structurally normal chromosomes. In Is(2L)/+ females, a high level of crossing over was due to extensive exchanges in the interstitial regions net-dp and dp and an increase in the number of tetrads with single exchanges. These changes resembled the IEC in rearranged chromosomes (in this case, in chromosomes bearing an insertion). Thus, the age changes of crossing over are similar to the consequences of the presence or absence of IEC. Age changes in crossing over in a chromosome depended both on the local rearrangements in this chromosome (the local effect on crossing over, LEC) and on rearrangements in nonhomologous chromosomes (IEC). In the first broods, both LEC and IEC decreased with an increase in the level of crossing over. In subsequent broods, the reduced level of crossing over was accompanied by an increase in both LEC and IEC. This suggests that the mechanisms responsible for the age changes in crossing over and IEC may have common steps. The contact model of crossing over may explain the similarity between the age changes in crossing-over and IEC. It is suggested that both phenomena result from delayed determination of crossing over in a meiotic cell. This may occur due to the retarded formation of the local contacts in one of the homologous chromosome pairs or because a higher number of local contacts is required to trigger crossing over in a meiotic cell (of early age).

Aging↗
PubMed1999

[Chromosome rearrangement: two ways of influencing crossing over in Drosophila].

Insertion of the Y-material into the 34A Is(Y;2L)419 region diminished recombinational length of the left arm of chromosome 2 (2L) from 49.1 to 15.0 cM. This decrease was compensated by the increase of recombinational length in the other chromosomal arms due to interchromosomal effect. The increase in the X chromosome was 11.4 cM; it was 2.0 cM in chromosome 2R; and 17.3 cM in chromosome 3. The insertion-induced decrease of the 2L recombinational length could be eliminated by evoking interchromosomal effects from other chromosomes. The presence of the inversion in the X chromosome increased the 2L recombinational length from 15.0 to 30.2 cM, while its association with the In(3LR)D inversion increased this length to 45.6 cM. The interchromosomal effects in the inductor chromosome were induced by distortion of pairing rather than by the low recombinational length of this chromosome. For example, the interchromosomal effect of the insertion on the X chromosome was higher in the Is(Y;2L)/+; In(3LR)/+ females than in the Is(Y;2L)/+; +/+ females (15.4 versus 11.5 cM), though the 2L recombinational length in the females with the former genotype (30.2 cM) was twofold higher than in females with the latter genotype (15.0 cM). It is suggested that chromosomal rearrangement hampers the development of local contacts in the homologues. This delay affects crossing over in the given pair of homologues in two ways: directly via diminishing the number of exchange sites, and indirectly through regulatory delay of crossing over determination in the meiocyte. The effects of the insertion on crossing over in nonhomologous chromosomes are implemented by through the second way.

Animals↗
PubMed1999

[The contact model of crossing over: definition of conditions required for the co-orientation of homologs].

Three phenomena have been examined: (1) independence of the segregation of structurally normal homologues from the position of crossover exchange relative to the centromere; (2) independence of chromosomal rearrangement ability to disturb disjunction from its position on chromosome; and (3) dependent, predominantly distal position of crossover exchanges in nondisjunction chromosomes. All three phenomena are explained in terms of the contact model of crossing over. According to the model, disjunction of the homologues is provided by a series of local contacts between them. The maximal number of contacts per arm is constant and is determined by the size of the absolute interference zone. The co-orientating influence of the contact decreases with the movement of its site away from the centromeric region responsible for the co-orientation. The role of the contact consists of bringing the centromeric regions of the homologues together. Co-orientation success does not depend on the presence or absence of a crossover exchange at the site of the contact. The nondisjunction chromosomes are selected with regard to the absence of proximal (or close to proximal) contacts. Hence, the exchanges formed on the basis of these contacts, are co-orientation-associated. In the disjunction chromosomes, the entire set of contacts is present. Any of these can be the first to develop and generate a crossover exchange. Because of this, exchanges in the disjunction chromosomes do not demonstrate association with the co-orientation. According to the model, the distortion of the previous contact disturbs (retards or prevents) the formation of the next contact. Hence, distortion of the contact formation in the site of rearrangement, irrespective to its location, would negatively affect the formation of the contact in the proximal region, and would promote nondisjunction.

Animals↗
PubMed1999

[Double crossing over: elementary events and the sequence of their occurrence].

Analysis of the crossing over increment in the structurally normal chromosome of Drosophila caused by a rearrangement in nonhomologous chromosome (interchromosomal effect on crossing over, IEC) was carried out based on the author's personal and literature data. The IEC in the left arm of chromosome 2 caused by inversions in chromosomes X and 3, as well as the IEC in X chromosome caused by inversions in chromosomes 2 and 3, were examined. The IEC-induced increment of crossing over results from the increase of the number of double exchanges under the constant or reduced number of single exchanges. Tetrad analysis showed that the given alternation of the crossing over processes could occur only in the case of conversion of the tetrads with single exchanges into the tetrads with double exchanges. In other words, the events leading to the formation of double exchanges occur consecutively. The borders of the IEC-induced double exchanges can be seen all over the chromosome body. However, the IEC-induced increase of chromosome recombination length occurs only in the proximal region (in rare cases, in proximal and distal regions) of the chromosome arm. This means that a double exchange is formed when the first event with predominant location in the middle of the arm is supplemented with the second event predominantly localized at the arm T end, most frequently in the proximal region. The pattern of the IEC-induced double exchange formation can be satisfactorily described in terms of the contact model of the crossing over. According to the model, an elementary crossing-over event is the local contact between the homologues. Neither single exchange nor a double-stranded DNA break can serve as an elementary event in the process of any multiple exchange formation.

Animals↗
PubMed1997

[Associated changes in recombination length, number of exchanges, and interference in Drosophila chromosome 2].

A set of eight strains differing in recombinational length of the left arm of chromosome 2(2L) was obtained by means of inserting genetic material of the Y chromosome into the 34A region and two inversions, In(1)dl-49 + BM1 and In(3LR)D, demonstrating interchromosomal effects on crossing over. The length of 2L ranged from 15.0 to 64.9 cM. Interchromosomal effects on crossing over differed in extent and in distribution over 2L between females carrying wild-type chromosome 2 and the chromosome with inserts. Tetrad analysis showed that the 2L recombinational length was increased up to the normal level (females +/+; +/+, +/+) or more due to increased proportions of single- or double-exchange tetrads, respectively. A model of pairing and crossing over proposed earlier was used to interpret crossing-over patterns. The model implies that initial pairing of homologous chromosomes involves the formation of local contacts between them. The number of exchanges in a bivalent is determined by the number of local contacts at the onset of an event termed the determination of crossing-over sites (DCS). Interference is determined by the mechanism of contact formation. The extent of interference varies both temporally and spatially (within a chromosome), decreasing from the periphery to a contact site as the time from contact formation increases.

Animals↗
PubMed1997

[A model of regulation of crossing over].

Very high variability is characteristic of crossing over. A mechanism of crossing-over variation is proposed on the basis of new data obtained by Chadov et al. Variations are believed to be determined by the character of pairing preceding crossing over and the mechanism of transforming contacts into exchanges. Pairing of homologues is assumed to involve consecutive formation of local contacts between them. The onset of this process depends of the chromosome structure. Exchanges appear in contact sites. Determination of crossing-over sites occurs when the contact number in a meiocyte reaches a certain threshold. The number of contacts formed in each chromosome pair by this time can vary. This results in variations of all parameters of crossing over: recombinational length (RL), exchange number per chromosome arm, and interference. The effect of a chromosome aberration on crossing over in aberrant and heterologous chromosome pairs, i.e., the interchromosomal effect on crossing over (IEC) and the mechanisms determining exchange number and interference, are explained on the basis of the proposed model.

Animals↗
PubMed1995

[Occurrence of chromosome aberrations in females heterozygous for deletion MS2-10: maternal effect].

The mutagenic effect of the paracentromeric heterochromatin deletion MS2-10 was studied in direct and reciprocal crosses of laboratory and wild-type lines of Drosophila melanogaster. The effect of deletion MS2-10 depended on the opposite chromosome. This was shown for the combination of autosome MS2-10 with autosome 2 from the Berlin wild line, but when MS2-10 was combined with an autosome from lines Canton S and pr pk cn, the effect was absent. When deletion MS2-10 was inherited from the female parent and the opposite chromosome from the male parent, the effect of the deletion was present, but it was absent in males heterozygous for MS2-10, obtained in reciprocal crosses. In maternal effect, this case of mutagenesis is similar to hybrid dysgenesis. However, the pattern of P-M dysgenesis was shown to differ from the type of mutagenesis described in the present work.

Animals↗
PubMed1995

[Crossing over in rearranged Drosophila chromosomes: the role of delayed pairing].

A Df(2R)MS2-10 deletion of pericentromeric heterochromatin, an Is(Y;2L)419 insertion of Y material in the region 34A, as well as nondisjunction of chromosomes 2 in 2/F(2L); F(2R) females did not directly prevent chromosome arms in chromosome 2 of Drosophila from pairing. However, these events resulted in (1) two- to four-fold decrease in the rate of crossing-over in chromosome 2;(2) a decreased proportion of exchange tetrads two to three times greater for multiple-exchange tetrads than for single-exchange ones; (3) and a decreased rate of crossing-over throughout the entire chromosome arm enhanced in a proximal direction, An In(l)dl-49+BMl inversion in the X chromosome cancelled the suppression of crossing-over. Crossing-over increased due to an increasing proportion of single-exchange tetrads. The changes in crossing-over found cannot be explained by asynapsis in the chromosomes with rearrangements. According to the authors, these changes are probably accounted for by a delayed pairing of these chromosomes. The delayed pairing of individual chromosome regions or the whole chromosome is considered the most common type of pairing disturbances. Its effect on meiosis are discussed.

Animals↗
PubMed1994

[The mechanism of the interchromsomal effect on crossing over in Drosophila melanogaster: delayed crossing over].

Interchromosomal effect on crossing-over (IEC) in autosome 2 has been studied in 2/F(2L); F(2R) females heterozygous for free arms (acrocentrics) and in Is(Y;2)419/+ females with an insertion of Y-material into the region 34A. IEC was induced by In(1)dl-49 + BM1 inversion. Manifestations of IEC included increased recombinational length of chromosome 2 and decreased interference. IEC was not observed in Df(2L)TW161/+ females with 38A-40 deletion. The patterns of IEC in three types of gametes of the 2/F(2L); F(2R) female depended on the pairing relations of the affected chromosome (chromosome-responder). In the case of normal pairing between the metacentric autosome 2 (the metacentric) and the F(2R) acrocentric, the increment in 2R length was minimal (20%), and the increment in the proportion of multiple-exchange (high-rank) tetrads (E2 + E3), maximal (8 to 10%). In the case of disturbed pairing 2-F(2R) nondisjunction, 2R length was increased by 77%, paralleled by a minimal increase in the proportion of high-rank tetrads (4%). Similarly, in females with the insertion, a pronounced increase in 2L length (74%) was associated with a moderate level of high-rank tetrads. When pairing in the chromosome-responder was normal, the increment in crossing-over was maximal in the pericentromeric region. In the case of disturbed pairing, this maximum either shifted toward the middle of the arm 2-F(2R) nondisjunction, or occupied a distal position (in females with the insertion). It is concluded that IEC pattern depends on the order of pairing in the chromosome-responder. The mechanism of IEC appears to be related to pairing "defects" within the responder. It is tempting to speculate that the onset of crossing-over is a whole-cell event, which is regulated by the overall level of chromosome pairing within the meiotic cell. Chromosomal aberrations increase the time required for attaining this level, and the start of crossing-over is delayed. As a result, (1) exchanges are observed in the regions of late synapsis, which are usually not involved in crossing-over; (2) overabundance of recombination enzymes, caused by delayed start of crossing-over, creates the conditions for decreased interference in paired regions.

Animals↗