The recombinational analysis of heterozygotes for a point-mutant N and a deficiency N suggests that the map region approximated by the interval fa to nd2 is at the right edge of salivary band 3C7 or in the interband to the right. The map region N55ell to fa can be anywhere between the left-interband and the right edge of 3C7. We discovered that small inversions also can be used in the recombinational analysis, and the inversion data support the conclusions already described. The reactivation of latent mutability in a Notch inversion resulted in reinversion of the original aberration, followed by reversion of N to N+. From the same Notch inversion, we isolated a spontaneous deficiency superimposed upon the original aberration, which supported our hypothesis that two of our w to N deficiencies probably originated as deficiencies superimposed upon inversions.
In the absence of assumptions pertaining to the organization and function of chromomeric DNA, the cytogenetic analysis of intragenic deletions that start at Notch and spread to the right or left of the locus suggests that the recombinational gene is bilaterally associated with salivary band 3C7. Either there are two genes resolved as a single cistron, or one must seek an alternative interpretation that allows some modicum of independent in the relationship between gene and band. Although we momentarily lean toward the hypothesis that gene and salivary band are separate entities on a binemic chromosome, alternative views can be devised, and the data must remain open to reinterpretation.—The recessive visible allele faswb behaves as a point mutant at the left end of the map and seems to be a deletion in the interval 3C6 to 7; we suspect some part of the band is missing. We have used the aberration in faswb as a cytological marker, isolated intragenic recombinants, and subjected them to examination. The analysis indicates that the chromosomal interchanges occurred to the right of 3C7.
Previous studies have indicated that recombination near the third chromosome centromere is associated with negative chromosome interference, a phenomenon for which GREEN (1975) and SINCLAIR (1975) suggested gene conversion as a possible mechanism. In this report, we demonstrate that negative chromosome interference is still observed when deficiencies or translocation breakpoints are scored as the middle markers in recombination experiments and the rate of recombination is increased by interchromosomal effect. We argue that these chromosomal rearrangement breakpoints are not subject to conversion. Since neither successive premeiotic and meiotic exchanges, nor negative chromatid interference, can by themselves account for the negative chromosome interference, we conclude that a greater than expected frequency of multiple exchanges actually occurs. We further suggest that negative chromosome interference may be characteristic of all chromosomal regions normally showing very little exchange in relation to physical length.
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