Abstract
Microspread pachytene nuclei of wild-type and W chromosome mutants of the mealmoth Ephestia kuehniella were used to study synaptonemal complex (SC) formation. In structurally heterozygous bivalents, axial elements of considerable length differences were brought to the same length by synaptic adjustment. The adjustment length was a compromise between the mutant and the wildtype homologue length in a structural heterozygote of a W chromosome-autosome translocation, T(A; W). The translocated non-homologous W segment really participated in SC formation as could be seen from the W chromosomal heterochromatin, used as a cytogenetic marker. Pachytene pairing of the wild-type W-Z bivalent extended from about two-thirds to the full length of the W chromosome, though from cytogenetic and genetic evidence W and Z are largely - if not completely - non-homologous. Nonhomologous pairing was even more conspicuous in sex chromosome bivalents containing a deleted W chromosome, Df(W). In one of the pairing configurations the halves of the Z chromosome were synapsed to either side of the Df(W). Thus, one side was pairing with the Df(W) in reversed order. The pairing behavior of the W with homologous chromosome segments was tested by introducing supernumerary W segments via the T(A; W) translocation. Pairing between the W and the translocated homologous W segment never occurred, whereas the Z frequently synapsed with it. Even in T(A; W) homozygotes, pairing between the two translocated W segments was not regularly found while the autosomal parts of the translocation chromosomes were always completely paired. Homologous chromosomes and the ability to form an SC are not sufficient for pairing initiation. Specific loci or sequences are postulated for this function. They are either absent from the W chromosome or are present in only low concentrations.
Original language | English |
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Journal | Chromosoma |
Volume | 94 |
Issue number | 2 |
Pages (from-to) | 125-131 |
Number of pages | 7 |
ISSN | 0009-5915 |
DOIs | |
Publication status | Published - 08.1986 |
Research Areas and Centers
- Academic Focus: Center for Infection and Inflammation Research (ZIEL)