Experimental alterations of the spores of lycopodium clavatum as related to diagenesis

Lycopodium clavatum spores have been heated to different temperatures at atmospheric pressure, at room temperature with 0.5 kbar pressure and at different temperatures with 1 kbar pressure, The effects of heat, pressure, and heat and pressure together on the spore have been examined in detail using different microscope techniques. Effects of some chemicals on these spores have also been observed.It is known that temperature and pressure change the colour of spore and pollen grain walls, mainly the exine (outer wall of the spore). Changes to the intine and the matter present in the cytoplasmic cavity (= inner contents), however, have not been taken into account by very many workers. In most of the previous works the inner contents were extracted before the experimental treatment began.In the present work, unextracted spores are used for the experiments which show two types of alterations of the spores with rising temperature at atmospheric pressure: (1) alteration of the inner contents, i.e. gradual colour change of the inner contents and their ultimate exudation from the spore through the exine at about 300°C; (2) gradual shrinkage of the exine due to the exudation of the inner contents which also causes an overall size reduction of the spore from 200° to 350°C. The exine does not change its colour up to 325°C; and this temperature, its starts to change its colour slowly, amalgamates with other exines of the empty spores, becomes amorphous, and ultimately deteriorates into unidentifiable organic matter.The process of colour change of the inner contents of spores and the general deformation are much slower when the spores are subjected to 1 kbar pressure with rising temperatures. Spores at room temperature with 0.5 kbar pressure show no colour change but only physical deformation.     

Comparative Expression Profiling Reveals an Essential Role for Raldh2 in Epimorphic Regeneration

Zebrafish have the remarkable ability to regenerate body parts including the heart and fins by a process referred to as epimorphic regeneration. Recent studies have illustrated that similar to adult zebrafish, early life stage larvae also possess the ability to regenerate the caudal fin. A comparative microarray analysis was used to determine the degree of conservation in gene expression among the regenerating adult caudal fin, adult heart, and larval fin. Results indicate that these tissues respond to amputation/injury with strikingly similar genomic responses. Comparative analysis revealed raldh2, a rate-limiting enzyme for the synthesis of retinoic acid, as one of the most highly induced genes across the three regeneration platforms. In situ localization and functional studies indicate that raldh2 expression is critical for the formation of wound epithelium and blastema. Patterning during regenerative outgrowth was considered to be the primary function of retinoic acid signaling; however, our results suggest that it is also required for early stages of tissue regeneration. Expression of raldh2 is regulated by Wnt and fibroblast growth factor/ERK signaling.     

Flavone-resistant Leishmania donovani Overexpresses LdMRP2 Transporter in the Parasite and Activates Host MRP2 on Macrophages to Circumvent the Flavone-mediated Cell Death

In parasites, ATP-binding cassette (ABC) transporters represent an important family of proteins related to drug resistance and other biological activities. Resistance of leishmanial parasites to therapeutic drugs continues to escalate in developing countries, and in many instances, it is due to overexpressed ABC efflux pumps. Progressively adapted baicalein (BLN)-resistant parasites (pB²⁵R) show overexpression of a novel ABC transporter, which was classified as ABCC2 or Leishmania donovani multidrug resistance protein 2 (LdMRP2). The protein is primarily localized in the flagellar pocket region and in internal vesicles. Overexpressed LdABCC2 confers substantial BLN resistance to the parasites by rapid drug efflux. The BLN-resistant promastigotes when transformed into amastigotes in macrophage cells cannot be cured by treatment of macrophages with BLN. Amastigote resistance is concomitant with the overexpression of macrophage MRP2 transporter. Reporter analysis and site-directed mutagenesis assays demonstrated that antioxidant response element 1 is activated upon infection. The expression of this phase II detoxifying gene is regulated by NFE2-related factor 2 (Nrf2)-mediated antioxidant response element activation. In view of the fact that the signaling pathway of phosphoinositol 3-kinase controls microfilament rearrangement and translocation of actin-associated proteins, the current study correlates with the intricate pathway of phosphoinositol 3-kinase-mediated nuclear translocation of Nrf2, which activates MRP2 expression in macrophages upon infection by the parasites. In contrast, phalloidin, an agent that prevents depolymerization of actin filaments, inhibits Nrf2 translocation and Mrp2 gene activation by pB²⁵R infection. Taken together, these results provide insight into the mechanisms by which resistant clinical isolates of L. donovani induce intracellular events relevant to drug resistance.