Role of the proneural gene, atonal, in formation of Drosophila chordotonal organs and photoreceptors

The Drosophila gene atonal encodes a basic helix-loop-helix protein similar to those encoded by the proneural genes of the achaete-scute complex (AS-C). The AS-C are required in the Drosophila PNS for the selection of neural precursors of external sense organs. We have isolated mutants of atonal, which reveal that this gene encodes the proneural gene for chordotonal organs and photoreceptors. In atonal mutants, all observable adult chordotonal organs, and almost all embryonic chordotonal organs fail to form; all adult photoreceptors are missing. For both types of sense organ, this defect is already apparent at the level of precursor formation. Therefore it is a failure in the epidermal-neural decision process i.e. a proneural defect. The failure to form photoreceptors results in atrophy of the atonal mutant imaginal disc, due to apoptosis and lack of stimulation of division. Lack of photoreceptors should also eliminate signalling that arises from differentiating photoreceptors and is required for morphogenetic furrow movement in the wild-type eye disc. Nevertheless, a remnant morphogenetic furrow is still observed in the atonal mutant disc. This presumably reflects the process of furrow initiation, which would not depend on signals from developing photoreceptors.

Stimulation of division in mouse 3T3 cells by coculture with embryonic chick limb tissue

Two regions of the chick limb bud — the apical ectodermal ridge and the zone of polarizing activity — have been shown to influence cell division and pattern formation during normal development and following surgical manipulation. In this study, using a simple coculture system, together with autoradiography, we have shown that these morphogenetically active regions of the limb bud can stimulate quiescent 3T3 cells to initiate DNA synthesis to a significantly greater degree than comparable but morphogenetically inactive regions of the limb bud.

PROLIFERATIVE RESPONSE OF THE SPLEEN AND LIVER TO HEMOLYSIS

Combined chemical and autoradiographic studies in rats injected with tritiated thymidine indicate that acute red cell sequestration stimulates reticuloendothelial (RE) proliferation. In the spleen DNA synthesis is most markedly stimulated in the marginal zone which is also the initial site of red cell sequestration. This proliferative response involves several division steps and eventuates in a colonization of the red pulp with increased numbers of all cell lines native to the spleen. In both spleen and liver there occurs also a generalized stimulation of division in the macrophages and littoral cells which involves only 1 or 2 division steps. Chronic compensated hemolytic anemia achieved in rats by injections of phenylhydrazine caused functional overactivity of the RE system, including increased sequestering function and hypergammaglobulinemia. This splenic hyperplasia did not entirely regress after cessation of the injections. In man the splenomegaly of a chronic non-immunological hemolytic anemia, hereditary spherocytosis, was found to involve a marked (average: 8-fold) hyperplasia of all spleen cellular elements. Neither the acute nor chronic proliferative reaction appears to arise from immunological or "toxic" stimuli and the findings support the view that the size of the RE system is a function of its particulate "work load." It is suggested that the cytoproliferative aspects of immune responses may depend upon non-specific, usually particulate stimulation. After prolonged stimulation, hyperplasia of the RES may become partly irreversible.