Transcription of X chromosomal DNA has been examined autoradio-graphically in various 1X2A and 2X2A normal larvae and 1X2A (+ X fr) and 2X2A (+ X fr) segmental aneuploid larvae of species Drosophila melanogaster. The segmental aneuploids contained duplications for the segment 9A–11A and 15D–ISA of the X chromosome. Results show that in the aneuploid male containing 9A–11A duplicaton both the homologous segments involved in the aneuploidy are autonomously hyperactive; their combined activity, measured by X/A grain ratio, is found to be nearly 70% more than the activity in normal male and about 100% more than that in diplo-X female. In the aneuploid female, containing the aneuploid segment 15D–18A and having three doses of the segment of the X chromosome, the activity was over 100% more than the diplo-X activity. The per gene dose activity for the two segments in the aneuploid male and female, respectively, is also significantly higher than their male and female counterparts. The possible role of lack of contiguity of the genetic segments and an intra-nuclear variation has been ruled out by appropriate analysis. We, therefore, interpret these findings to be due to an autonomous expression of the X linked compensatory genes, resulting from a primary modulation in the organization of the entire X chromosome. The autosomal signal then renders the individual genetic locus hyperactive.

The Tcp-1 gene is located within the t complex and codes for a major testicular cell protein called p63/6.9. All wild-type chromosomes carry the Tcp-1b allele which codes for a basic form of this protein, while all complete t haplotypes carry the Tcp-1a allele which codes for an acidic form of this protein. It is not clear whether the Tcp-1 gene is associated with phenotypic effects of t haplotypes on embryogenesis and/or spermatogenesis, since the genetic basis for these effects is extremely complex. The elegant analysis of Lyon & Mason (1977) has allowed the identification and separation of a family of genetic factors which interact to produce the observed phenotypes associated with various combinations of t haplotypes. The data summarized in this report indicate that the Tcp-1a locus is separable from all of the identified t haplotype factors except for one; a complete correlation has been obtained between Tcp-1a and a proximal t haplotype factor which is involved in effects on transmission ratio distortion. Two other novel points emerge from this analysis. First, it appears that the tail interaction factor and the proximal sperm factors represent distinct genetic loci. Second, the accumulated data lead to the proposal that the TOrl chromosome carries a short segment of t haplotype chromatin containing Tcp-1a and proximal sperm factors involved in transmission ratio distortion and sterility.

A comparative study of two male recombination factors (31. 1 MRF and 23. 5 MRF) isolated from the same Southern Greek natural population, revealed specific differences in their activities. 23. 5 MRF induces female sterility due to atrophie ovaries at a wide range of temperatures while 31. 1 MRF does so only at high temperatures. The gross morphology of the atrophie ovaries was the same and unilaterally affected pairs were found in the F1 of crosses with both 23. 5 and 31. 1 MRF. Furthermore, 23. 5 MRF induces: (a) lower frequencies of abnormal anaphases I and II than 31. 1 MRF, (b) higher frequencies of ‘double crossovers’ resulting from deficiences or duplications, (c) large clusters of recombinants, suggesting premeiotic origin and (d) cases where one of the non-recombinant phenotypes was not produced. Such cases have never been observed with 31. 1 MRF. Moreover, the cytoplasm of the Cy L4/Pm strain that suppresses 31. 1 MRF does not affect the activities of 23. 5 MRF. Hypotheses to explain the different behaviour of the two factors are presented and discussed.

Electrophoretic surveys for nine species of Drosophila have been summarized in terms of the relative contribution to heterozygosity of each of ten gene frequency classes, the mean frequency of heterozygotes within subpopulations, and the degree of genetic divergence between subpopulations. It has been shown that the neutral model proposed by Kimura, and modified by Ohta to include the accumulation of slightly disadvantageous mutations, is capable of explaining all features of the data. The consistent difference between group I and group II enzymes can be explained by a difference in the average intensity of selection against mutational variants in the two groups. A highly significant difference between the temperate and tropical species in the distribution of heterozygosity appears to be due to the smaller effective breeding population sizes in the case of the temperate species.

Selection was carried out in mice for concentration of thyroxine hormone (T4) in plasma of males at 11 weeks of age over seven generations. Selection was practised for high level in two replicate lines and for low level in two replicate lines, and there was an unselected control. There was a response in both directions, and the divergence of 12·4 ng/ml observed in generation seven was equivalent to about 20% of the base population mean or nearly one phenotypic standard deviation. The realised heritability was 9%.

Plasma thyroxine level had a repeatability of 0·54 when two measurements were made 24 h apart. The responses made at 11 weeks in males were also evident in both males and females at 5 weeks. Plasma tri-iodo thyronine (T3) concentrations showed a correlated response almost as large, relative to the mean level, as that in T4.

Positive correlated responses were observed in total weights of the litter at 12 days, and in individual weights at 3, 6 and 9 weeks, the responses in the early weights being greater relative to their mean. The results suggest that the correlated weight changes were due to genetic responses in maternal characteristics, probably milk production, rather than individual growth.

Interest in the selection of mutations affecting L-proline catabolism in Aspergillus nidulans is heightened by the involvement of one of the very few examples of a cluster of functionally related genes in an eukaryote and by an increasing awareness of the biological phenomena in which proline and proline catabolism participate. The sasA-60 (semialdehyde sensitive) mutation in A. nidulans results in toxicity of catabolic precursors of L-glutamic γ-semialdehyde (or its internal Schiff base L-Δ1-pyrroline-5-carboxylate) and succinic semialdehyde, apparently without affecting the catabolic pathways concerned. As sasA-60 is unlinked to the prn gene cluster, specifying the gene products necessary for L-proline catabolism and as L-proline, a precursor of L-glutamic γ-semialdehyde, is highly toxic to sasA-60 strains, this forms the basis of a powerful positive selection technique for obtaining a number of types of prn mutations. Many of these prn mutations can be directly classified according to the gene product(s) affected on the basis of growth phenotype with respect to L-arginine and L-ornithine utilization, proline-dependent resistance to certain toxic amino acid analogues and effect on supplementation of proline auxotrophies. The availability of both a positive selection technique and an extensive nutritional screening system has enabled the identification of fourteen spontaneous deletion mutations, recognized as extending into the prnB gene, specifying the principal L-proline permease, and into at least one other prn gene. These deletion mutations have been partially characterized both genetically and biochemically. In particular their use has greatly facilitated fine-structure mapping of the prn cluster and aided studies of the regulation of prn gene expression.

Genetic analysis of 12 mutants of Escherichia coli K12 defective in D-alanine dehydrogenase showed that alnA and dad are alternative names for the same locus. dad was shown to be a single gene which codes for a protein of 55000–60000 mol. wt. Study of thermosensitive mutants of dad indicated that its product is a structural component of D-alanine dehydrogenase. The regulatory gene alnR was shown to be involved in positive control of dad expression. This was concluded from (i) the absence of constitutive strains among Dad+ revertants of alnR– mutations, (ii) the trans dominance of alnR+ to alnR–, and (iii) the failure to isolate fully constitutive strains by any means. To obtain a uniform nomenclature it is proposed to re-name dad as dadB and alnR as dadQ.