IIIRa is a genetic modifier of Segregation Distortion (SD) in Drosophila melanogaster, which was discovered in the same natural population from Ranna (Sicily) that carried SDRa. It is located at 49·7 ± 0·8 on chromosome III. IIIRa was found to have a dominant effect on segregation distortion which varied with the origin of the SD chromosome tested. Thus it enhanced the level of distortion caused by 14 SD chromosomes from seven natural populations in Southern Italy and Sicily, but decreased the level of distortion caused by SDR−1, a chromosome from a natural population near Rome. Moreover, IIIRa determined or enhanced the distorting effect of SDRa in males heterozygous for SDRa and various SD+ wild chromosomes differently sensitive to SDRa. The frequency of chromosomes having an effect like IIIRa chromosome was very high (around 70%) in samples from two natural populations of Southern Italy tested-those of Ranna and Corato. No effects of IIIRa other than its ability to modify SD have been detected.

Single-point crosses using five allelic spore colour mutants at the buff locus were carried out at different temperatures. The data suggest (i) that fixed or preferred opening points in the DNA, required for initiation of recombination events, are available more often at higher than at lower temperatures, (ii) opening points at or beyond both proximal and distal ends of the buff locus respond similarly to variations in temperature, and (iii) the correction pattern seems to be independent of temperature at the buff locus in S. brevicollis.

DNA prepared from transformed stocks of Drosophila melanogaster induces second-step transformations resembling the original. The gross yield of transformants induced by transformed DNA is several times higher than that induced by the original allo-DNA, but much of this high frequency is attributable to a few exceptionally large clusters of transformants among flies treated with transformed DNA. When these large clusters are omitted from the data, the frequency of transformants induced by DNA from transformed stocks is the same as that induced by allo-DNA. The data therefore support the conclusion that the original DNA-induced alterations resulted from the transfer of genetic material capable of indefinite replication.

When the mutant veinlet was removed from a Drosophila melanogaster line selected for shortened vein length it was found that the selected polygenic background produced vein gaps in the absence of the major mutant. This example of genetic assimilation was unusual, however, in that the phenotype of the assimilated line was not exactly the same as the phenotype of the original selection line. It differed in two respects: only one of the longitudinal veins was affected in the assimilation line whereas all veins are shortened in the selected ve line, and vein gaps were sub-terminal in the assimilated line whereas they are terminal in veinlet. Modifiers of L 4 vein length were found to be located on both chromosomes II and III, though the chromosome II factor had a larger effect and was required for gap formation. The chromosome II gene was mapped to the same position as a similar L 4 vein length polygene (PL(2)L4a) found in another veinlet selection line and reported elsewhere. The pattern of expression of the ve mutant and the assimilated line genotype were compared using profiles of vein frequency at given points. The vein pattern profiles are discussed in relation to an hypothesis to explain the observed selection response and the effectiveness which these polygene combinations showed in modifying the much more complex veinlet phenotype.

Purine auxotrophs of Micrococcus luteus were induced by N-methyl-N′-nitro-N-nitrosoguanidine. They were biochemically characterized by growth stimulation with CO2-enriched air and purine intermediates and by the Bratton-Marshall test that is used to detect accumulated diazotizable amines. The mutants were divided into four classes: pur (EC), purH, purJ, and Pur−. The pur(EC) class was further subdivided into purE and purC by results of crossing all the pur(EC) mutants with a known purE reference strain (ATCC 27141). Mutants which were not linked to the reference purE marker were considered to be purC. Genetic mapping was accomplished by using two-point reciprocal transformation crosses. The result of this study indicates that purJ mutants may be loosely linked to purE and purC, and purH mutants are not linked to purE, purC or purJ.

Recombination in a short genetic interval spanning the proximal region of chromosome 3 was studied in the regions st-in-ri-eg2-Ki-pp. Crossover frequencies in this region varied considerably in different genetic backgrounds; however, in all genotypes, the following observations were made: (1) an excess of multiple recombinant chromosomes indicative of high negative interference, was detected; (2) among the multiple recombi-nants, a positive correlation of simultaneous exchange in the most proximal and shortest adjacent genetic intervals was noted; (3) several classes of reciprocal products were not equally recovered. Three possible explanations for these results are: pre-meiotic exchange, chromatid interference and gene conversion.

The alcohol dehydrogenase (ADH), glutamate oxaloacetate transaminase (GOT), acid phosphatase (ACPH), endopeptidase (EP) and aminopeptidase (AMP) zymogram phenotypes of Chinese Spring wheat, Imperial rye, the Chinese Spring-Imperial triticale and the series of seven disomic Imperial chromosome additions to Chinese Spring were determined. It was found that the zymogram phenotypes produced for one or more of the enzymes by each of the Imperial chromosomes 3, 6, C and D differ sufficiently from that of Chinese Spring so as to provide evidence for the presence or absence of each of these chromosomes in addition lines and triticales. The structural genes Got-R2 and Got-R3 were located in Imperial chromosomes 6 and 3 respectively and other genes involved in the production of GOT in chromosomes C and D. By analysis of GOT alone, evidence for the presence or absence of Imperial chromosomes 3, 6, C and D in addition lines and triticales can be obtained. Adh-R1 was located in chromosome C and a gene(s) involved in the production of an ACPH was located in chromosome D.

The linkages obtained for Got-R2, Got-R3 and Adh-R1 demonstrate homoeology between the Imperial chromosomes 3, 6 and C and the Chinese Spring chromosomes of groups 3, 6 and 4 respectively. The discovery that Adh-R1 is located in Imperial chromosome C also suggests that the 4R/7R and 7R/4R homoeologous groupings proposed elsewhere for the chromosomes of the rye cultivars Imperial, Dakold, and King II should be reassessed, since they are inconsistent with the known linkages of Adh-R1 in the three cultivars. The finding in King II of two forms of ADH and of two ADH genes has been reported. The results of our study of Imperial, King II, and Dakold indicate that rye possesses but one ADH and only one ADH structural gene.

Linkage data for the following markers on chromosome 17 of the house mouse were obtained: centromere (marked by translocation R67), Brachyury (T), tufted (tf), H-2, and thin fur (thf). The markers were found to be arranged in that order in the genetic map and the combined genetic distances between individual markers were found to be as follows: Rb7…T, 4·5 cM; T…tf, 5·8 cM; tf…H-2, 5·0 cM; H-2…thf, 15·1 cM. The localization of the thf locus on the non-centromeric side of the H-2 complex provides an important marker for this arm of chromosome 17. The map distances in the centromeric portion of chromosome 17 changed drastically in the presence of various t factors. These factors strongly reduce the recombination frequency in the T…tf and tf…H-2 intervals and this crossing-over suppression is most likely responsible for the linkage disequilibrium between t and H-2 reported earlier. Recombinants involving a t chromosome but occurring to the right of the H-2 complex do not change the properties of t factors suggesting that all determinants responsible for the t phenotype are located in the chromosomal region between T and tf (H-2).

Improvements in cytotoxic technique allowed a determination to be made of the strain distribution and inheritance of Mph-1, the mouse peritoneal exudate cell alloantigen. Mph-lb, the allele in B10 lines, is inherited as a Mendelian co-dominant gene. In a 3-point backcross using the colour markers pink eye dilution (p) and chinchilla (cch) it was shown to map about 36 units from p in the order p-cch-Mph-l on chromosome 7. An alternative antigen, Mph-1.1, has been identified on strains F/St and I/StDa.