Analysis of the autosomal mutation abo and its interaction with the ribosomal DNA or Drosophila melanogaster: the role of X-chromosome heterochromatin.

The autosomal recessive, maternal-effect mutation abnormal oocyte (abo: 2-38) preferentially lowers the viability os XO progeny. The severity of the sex-ratio distortion is reduced by duplications of maternal or zygotic heterochromatin (SANDLER 1970, 1977; PARRY and SANDLER 1974). Utilizing X-chromosome inversions that contain modifications in the quantity and arrangement of the heterochromatic functions, Xhabo and cr+, wer have extended our investigations of abo's influence on XO male recovery and rDNA redundancy (KRIDER, YEDVOBNICK and LEVINE 1979).--XO males bearing In(1)SCS1LSC4R or In(1)Wm4LSC4R are recovered twice as frequently as X chromosomes containing a single Xh region, implying that these inversions possess a duplication of Xhabo. abo mutant females heterozygous for In(1)SCS1LSC4R and wild-type X chromosomes generate XO progeny that do not contain elevated rDNA redundancies. XO males containing In(1)Wm4 exhibit male recoveries and rDNA elevations similar to those of males bearing a wild-type X chromosome, when both derive from a common abo/abo mother. Reciprocal crosses baetween In(1)Wm4 and Canton-S males to attached-X abo females show significant, though reuduced, sex ratios in the absence of an rDNA effect. The observation that abo can elevate the rDNA redundancy of In(1)Wm4, a chromosome that does not compensate, suggests that abo and cr+ functions are not directly related.

The effect of abo phenotypic expression on ribosomal DNA instabilities in Drosophila melanogaster.

The recessive maternal-effect mutation, abnormal oocyte (abo:2--38), reduces viability in the offspring of homozygous mutant females. Zygotes lacking specific heterochromatic segments of the X or Y chromosomes are most severely affected. We have shown that abo/abo lines can lose the capacity to express the mutant phenotype, and that elevated rDNA redundancies can be observed in such stocks (Krider and Levine 1975). In this study, we describe a microhybridization procedure that facilitates the measurement of rDNA redundancy, using a small number of adult Drosophila. We show that instability of the rDNA content persists in an abo/abo line after loss of the capacity to express the phenotype, and that changes in rDNA amounts occur between successive generations of the stock. Further, we show that the rDNA content of XO progeny from abo/abo females is elevated. The effect is directly correlated with the expression of the abo phenotype, and it is not observed in the XO progeny of abo heterozygous females or abo homozygotes from lines that do not show abo expression.

Studies on the mutation abnormal oocyte and its interaction with the ribosomal DNA of Drosophila melanogaster.

Sandler (1970) suggested that mutation, abnormal oocyte (abo:2-38), may influence the function of the ribosomal RNA cistrons. We have examined the abo mutation and its interaction with the ribosomal DNA of Drosophila melanogaster. We observed that the expression of the abo phenotype is unstable under the appropriate conditions, a behavior which paralleled changes in the phenotypic expression of bobbed mutations during the magnification of the ribosomal DNA. The change in the expression of the abo phenotype is correlated with an increase in the redundancy of the ribosomal cistrons, further suggesting a functional interaction of the abo and bobbed regions.

Uptake of catecholamines in guinea pig lung: influence of cortisol and anaphylaxis.

UNLABELLED: Effects of cortisol and anaphylaxis on the uptake of catecholamines (CA) in the guinea pig lung have not been investigated previously. Sensitized and healthy animals were randomly killed, catheters were inserted into the pulmonary artery and vein, and the preparation was perfused with Tyrode. Half of the animals received 50 mg. of cortisol 2 hours before the procedure. H3-epinephrine (E) or norepinephrine (NE), 10 ng. per milliliter, was infused for 6 minutes. Infusion was started 15 seconds prior to challenge with ovalbumin or NaCl. Total -H3 and NE(E)-H3 were determined in the lung homogenates. Results showed (1) 6 to 14 per cent of circulating CA were retained by the lung. (2) In healthy animals cortisol inhibited NE uptake by 35 per cent and E uptake by 15 per cent. (3) Anaphylaxis increased NE and E accumulation by 10 and 19 per cent, respectively. (4) Regardless of experimental conditions approximately 40 per cent of NE and 30 per cent of E taken up were recovered unchanged. IN CONCLUSION: (1) There is significant uptake of CA in the lung. (2) One of the mechanisms of therapeutic effect of cortisol in asthma might be its inhibitory effect on CA uptake. (3) Increased CA accumulation during anaphylaxis could be beneficial by increasing the local concentration of amines, or detrimental by decreasing availability of CA, depending on the uptake site and cell type and degree of subsequent metabolism. (4) Cortisol and anaphylaxis per se appear not to change degradation of CA.