RFLP approach to breeding for quantitative traits in plants—a critique

A number of recent papers suggest that use of RFLPs as markers offers a clear advantage in breeding for improvement in quantitative traits (QTs). The concepts underlying establishment of linkage between RFLP markers and QT loci stem from three papers on tomato published during 1987–1991. Essentially, continuously varying QT phenotypes are assigned to RFLP genotype classes, which can be considered to be determined by a single, diallelic gene with codominant alleles. Linkage is inferred through statistical analysis. Similarly, interaction between markers and QT is also tested by an analysis of variance. Here, the statistical methods employed in these three papers to detect linkage are critically evaluated, especially because subsequent investigations take the concepts developed in these papers as proven. In this paper, we examine the three fundamental papersde novo. We scrutinize the methods employed and the inferences drawn to bring to light what we believe are conceptual drawbacks

The Indian Plant Variety Protection Act Beneficiaries: The Indian Farmer or the Corporate Seed Company?

506-515The Indian Plant Variety Protection (PVP) Act (2001) covers several issues relating to farmers’ rights and the protection and registration of new plant varieties. It is a sui generis system developed after years of deliberation and offers tremendous freedom to farmers to continue saving and reusing seeds from their farm produce. As Indian farmers fall into diverse socio-economic classes, all of them will not benefit equally from the PVP Act. PVP issues relating to farmers’ rights are discussed vis-à-vis their role in biodiversity conservation and plant breeding. Possible solutions to mitigate the drawbacks of long-term protection to farmers are also discussed

Mutants dissecting development and behaviour in Drosophila

We have traced in this paper the progress in Drosophila genetics research from the 1960s, at the IARI, spearheaded by the visionary insight of M. S. Swaminathan. The work started with the study of indirect effect of radiation and the synergistic interaction of physical and chemical mutagens on chromosomal and genetic changes. This paved the way for the study of single gene mutants in dissecting developmental and behavioural processes. New genes discovered by us have been shown to encode conserved cell signalling molecules controlling developmental and behavioural pathways. With the complete sequencing of the Drosophila genome, in the year 2000, mounting evidence for the homology between Drosophila and human genes controlling genetic disorders became available. This has led to the fly becoming an indispensable tool for studying human diseases as well as a model to test for drugs and pharmaceuticals against human diseases and complex behavioural processes. For example wingless in Drosophila belongs to the conserved Wnt gene family and aberrant WNT signalling is linked to a range of human diseases, most notably cancer. Inhibition as well as activation of WNT signalling form the basis of an effective therapy for some cancers as well as several other clinical conditions. Recent experiments have shown that WNTs might also normally participate in self-renewal, proliferation or differentiation of stem cells and altering WNT signalling might be beneficial to the use of stem cells for therapeutic means. Likewise, the stambhA mutant of Drosophila which was discovered for its temperature-dependent paralytic behaviour is the fly homologue of Phospholipase Cβ . Phospholipase C mediated G protein signalling plays a central role in vital processes controlling epilepsy, vision, taste, and olfaction in animals. Proteins of the G-signalling pathway are of intense research interest since many human diseases involve defects in G-protein signalling pathways. In fact, approximately 50% of the drugs used in clinical medicine target cellular pathways containing G-protein signalling elements. The detailed study of PLC-dependent G protein signalling in Drosophila is bound to throw light on the role of G protein-mediated biological functions and on similar genes and their functions in human diseases

Drosophila mutants in phospholipid signaling have reduced olfactory responses as adults and larvae

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 Gqα and phospholipase Cβ 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 Gqα and Plcβ21c, and modulated by the stmA gene product

Chromatin remodeling protein INO80 has a role in regulation of homeotic gene expression in Drosophila

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