The homologues of yeast INO80 are identified across phyla from Caenorhabditis elegans to human. In Drosophila it has been shown that dINO80 forms a complex with Pleiohomeotic but does not interact with Hox PRE (polycomb responsive element). As some proteins of the INO80 complex are implicated in homeotic gene regulation, we examined if dINO80 is involved in regulation of homeotic genes. We find that dINO80 null mutants generated by imprecise excision of P-element are late embryonic lethals and show homeotic transformation. We detect misexpression of homeotic genes like Sex-comb reduced, Antennapedia, Ultrabithorax and Abdominal-B in dIno80 mutant embryos by immunostaining which is further substantiated by quantitative PCR. Polycomb phenotype in dIno80-Pc is enhanced in double mutants. Concurrently, the localization of dINO80 to sequences upstream of misexpressed genes in vivo shows that dINO80 is involved in homeotic gene regulation and probably through its interactions with PcG-trxG complexes.

Somatic chromosome number and detailed karyotype analysis were carried out in six Indian Momordica species viz. M. balsamina, M. charantia, M. cochinchinensis, M. dioica, M. sahyadrica and M. cymbalaria (syn. Luffa cymbalaria; a taxon of controversial taxonomic identity). The somatic chromosome number 2n = 22 was reconfirmed in monoecious species (M. balsamina and M. charantia). Out of four dioecious species, the chromosome number was reconfirmed in M. cochinchinensis (2n = 28), M. dioica (2n = 28) and M. subangulata subsp. renigera (2n = 56), while in M. sahyadrica (2n = 28) somatic chromosome number was reported for the first time. A new chromosome number of 2n = 18 was reported in M. cymbalaria against its previous reports of 2n = 16, 22. The karyotype analysis of all the species revealed significant numerical and structural variations of chromosomes. It was possible to distinguish chromosomes of M. cymbalaria from other Momordica species and also between monoecious and dioecious taxa of the genus. Morphology and crossability among the dioecious species was also studied. Evidence from morphology, crossability, pollen viability and chromosome synapsis suggests a segmental allopolyploid origin for M. subangulata subsp. renigera. The taxonomic status of the controversial taxon M. cymbalaria was also discussed using morphological, karyological and crossability data.

In this paper, we show that mutants in the gene stambhA (stmA), which encodes a putative phosphatidylinositol 4,5 bisphosphate-diacylglycerol lipase, exhibit a significant reduction in the amplitudes of odor-evoked responses recorded from the antennal surface of adult Drosophila. This lends support to previously published findings that olfactory transduction in Drosophila requires a phospholipid intermediate. Mutations in stmA also affect the olfactory behavior response of larvae. Moreover, there is a requirement for G(q)alpha and phospholipase Cbeta function in larval olfaction. The results suggest that larval olfactory transduction, like that of the adult, utilizes a phospholipid second messenger, generated by the activation of G(q)alpha and Plcbeta21c, and modulated by the stmA gene product.

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The mutant stambhA1 (2-56.8) of Drosophila melanogaster was identified as a reversible temperature sensitive adult and larval paralytic. We have (i) isolated and analysed phenotypes of one new homozygous viable paralytic allele and two recessive unconditional embryonic lethal alleles of stmA and (ii) studied the interaction of the viable paralytic alleles with ts paralytic mutants napts1 (2-55.2) and parats1 (1-53.9). The homozygous viable paralytic alleles stmA2 and stmA1 are semi dominant neomorphs. The lethal alleles stmA12 and stmA7 appear to be amorphs. Unhatched embryos expressing lethal stmA alleles showed hypotrophy of the anterior dorsal cuticle overlying the brain with a concomitant hypertrophy of the anterior dorsal neurogenic region (the brain). The ventral cuticle was poorly differentiated, and the ventral nerve chord showed mild hypertrophy and poor organisation. The epidermal cells in 12-13 h old embryos did not show the normal palisade layer arrangement. These phenotypes are similar to mutant phenotypes of the neurogenic class of genes whose wild type functions are necessary for intercellular communication. The alleles stmA1 and stmA2 do not appear to interact with the paralytic mutants napts1 or parats1 in double mutant combinations. On the basis of our results it is proposed that stmA may belong to the neurogenic class of genes.