PubMed Health⌕ Search

PubMed · 9178019

Conditions for protected inversion polymorphism under supergene selection.

Abstract

Conditions for protected inversion polymorphism under the operation of both karyotype and supergene selection in a viability model have been analytically determined. When supergene selection (the effect of recombination in homokaryotypes lowering the mean fitness of their offspring) is acting on gene arrangements and there is no karyotype selection, it is demonstrated that a polymorphic stable equilibrium is reached by the population, which is a function of only the recombination effects in homokaryotypes. Under both supergene and karyotype selection the degree of dominance (h) of karyotype selection is critical to produce a protected inversion polymorphism. In general, the opportunity for protected polymorphism increases as the degree of dominance decreases. For small s values, the conditions for protected polymorphism are r > 2sh and c > 2s(h-1), where r and c are the average loss of viability for offspring of ST/ST and IN/IN homokaryotypes, respectively. These findings suggest that supergene selection may be an important balancing mechanism contributing to the maintenance of inversion polymorphism.

Explore related subjects

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

G Alvarez, C Zapata. 1997. Conditions for protected inversion polymorphism under supergene selection.. https://doi.org/10.1093/genetics%2F146.2.717

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related citations

Detection and quantification of CBFB/MYH11 fusion transcripts in patients with inv(16)-positive acute myeloblastic leukemia by real-time RT-PCR.

We used a newly established real-time RT-PCR assay for the quantification of the leukemia-specific CBFB/MYH11 transcripts in inv(16)-positive acute myeloblastic leukemia. CBFB/MYH11 could be quantified over a five log range, with a detection limit of 10 molecules of a CBFB/MYH11 plasmid and a 1:10(5) dilution of RNA of the inv(16)-positive ME-1 cell line, respectively. The fusion transcripts were also quantified in 19 patients with acute myeloblastic leukemia and an inv(16) at initial diagnosis. The expression of CBFB/MYH11 varied over a two log range without correlation to clinical response or relapse rate. In nine patients, CBFB/MYH11 was also quantified during/after chemotherapy and autologous or allogeneic stem cell transplantation. All of these patients showed a similar decline of CBFB/MYH11 after intensive therapy. Six of these patients are in complete remission with a stable low-level or absent CBFB/MYH11 expression. Three patients relapsed, and their CBFB/MYH11 transcripts rose again to pretreatment levels. In two patients, this increase in CBFB/MYH11 could be detected by real-time PCR before hematological relapse. These data indicate that real-time RT-PCR can be used for the sensitive detection and quantification of CBFB/MYH11 transcripts in the follow-up of patients with inv(16)-positive AML.

Chromosome Inversion↗

Bad neighbors.

Explore the source record for details and available documents.

Chromosome Inversion↗

Transcriptional activity of an inversion split NOR in barley (Hordeum vulgare L.).

The transcriptional activity of NORs in a new structural mutant of barley (PK-88-4) was studied based on the positive reaction of NORs of metaphase chromosomes with AgNO3 and the number and size of silver-stained nucleoli in somatic interphase cells and meiocytes. PK-88-4 proved to contain a pericentric inversion that split NOR 7 into two unequal parts residing in the opposite arms of the reconstructed chromosome 7(5). This chromosomal rearrangement enables testing of intrachromosomal suppression of NORs and provides insight into the mechanisms of intraspecific nucleolar dominance. Both parts of the split NOR proved to be transcriptionally active, and are not subject to intrachromosomal nucleolar dominance. Thus, translocation-induced intraspecific nucleolar dominance is probably the result of interaction of NOR6 and NOR7 or other genetic factors located on the NOR-bearing chromosomes 6(6H) and 7(5H).

Chromosome Inversion↗