Male killing bacteria such as Spiroplasma are widespread pathogens of numerous arthropods including Drosophila melanogaster. These maternally transmitted bacteria can bias host sex ratios toward the female sex in order to ‘selfishly’ enhance bacterial transmission. However, little is known about the specific means by which these pathogens disrupt host development in order to kill males. Here we show that a male-killing Spiroplasma strain severely disrupts nervous tissue development in male but not female D. melanogaster embryos. The neuroblasts, or neuron progenitors, form properly and their daughter cells differentiate into neurons of the ventral nerve chord. However, the neurons fail to pack together properly and they produce highly abnormal axons. In contrast, non-neural tissue, such as mesoderm, and body segmentation appear normal during this time, although the entire male embryo becomes highly abnormal during later stages. Finally, we found that Spiroplasma is altogether absent from the neural tissue but localizes within the gut and the epithelium immediately surrounding the neural tissue, suggesting that the bacterium secretes a toxin that affects neural tissue development across tissue boundaries. Together these findings demonstrate the unique ability of this insect pathogen to preferentially affect development of a specific embryonic tissue to induce male killing.

Two pathways have been postulated for the conversion of propionic acid to pyruvic acid by liver mitochondria. Mahler and Huennekens (1953) suggested that propionic acid was oxidized to acrylic acid which was converted to pyruvic acid through Land D-lactic acids. The alternative pathway involves a direct carboxylation of propionic acid to succinic acid (Lardy and Adler, 1956; Flavin et al., 1955). An enzyme system which catalyzes the carboxylation of propionic acid has been demonstrated in Propionibacterium pentosaceum (Barban and Ajl, 1951), Chlorobium thiosulfatophilum (Larsen, 1951), Micrococcus lactilyticus (Whiteley, 1953) and Veillonella gazogenes (Delwiche et al., 1954). Cells of a thiamin deficient Nocardia corallina oxidized propionic acid to pyruvic acid which accumulated in the system. This communication includes results which suggest that two pathways operate in N. corallina for the oxidation of propionic acid. METHODS N. corallina strain S was isolated by Batt and Woods (1951) and a growth requirement for thiamin was shown for the organism by Martin and Batt (1957).

The nutritional requirements of Streptothrix corallinus (Nocardia corallina, Breed et al., 1948) were studied by Reader (1928) who showed that growth in a medium containing glucose, ammonium sulfate and inorganic salts was stimulated by the addition of small amounts of tryptic meat broth or yeast extracts. The active principle in these additions was thought to be related to, but not identical with, vitamin B1 (Peters et al., 1928). Lutz (1948a) showed that the thiamin requirement of Mycobacterium agreste (N. corallina, Breed et al., 1948) could be replaced by 2methyl-4-amino-5 aminomethyl pyrimidine. This communication deals with the growth factor requirements of N. corallina (strain S) isolated by Batt and Woods (1951).