Diurnal regulation of plastid genes in Populus deltoides.

Light regulates leaf and chloroplast development, together with overall chloroplast gene expression at various levels. Plants respond to diurnal and seasonal changes in light by changing expression of photosynthesis genes and metabolism. In Populus deltoides, a deciduous tree species, leaf development begins in the month of March and leaf maturation is attained by summer, which is subsequently followed by autumnal senescence and fall. In the present study, diurnal changes in the steady state transcript levels of plastid genes were examined in the fully developed leaves during summer season. Our results show that steady state level of the psaA/B, psbA, psbEFLJ and petA transcripts showed differential accumulation during diurnal cycle in summer. However, there was no significant change in the pigment composition during the day/night cycle. Our studies suggest that the diurnal regulation of steady state mRNA accumulation may play a crucial role during daily adjustments in plants life with rapidly changing light irradiance and temperature.

Ascorbic acid metabolism in ageing recalcitrant sal (Shorea robusta Gaertn. f.) seeds.

Changes in ascorbate content and its enzymatic utilization pattern were studied in embryonic axes and cotyledons of sal seeds undergoing rapid loss of viability, at ambient conditions. Ascorbate levels were significantly higher initially in the embryonic axes (0.32 mg/g fresh weight) and cotyledons (0.21 mg/g fresh weight) of freshly mature, relatively hydrated (42.2% moisture content) and 100% viable sal seeds. It declined sharply as the tissues; embryonic axes and cotyledons, desiccated with absolutely no detectable amount in non-viable seeds (21% moisture content). Significantly strong correlation was obtained between desiccation of embryonic axes (r = 0.96) and cotyledon (r = 0.97) with loss of ascorbate levels and loss of germinability. Higher rates of ascorbic acid utilization (AAU) recorded in the embryonic axes of 100% viable seed declined sharply as the seed viability reduced due to desiccation below 36.8% moisture content. AAU was not detected in the cotyledons.

Subgroup-A Rous sarcoma virus-induced growth stimulation of chick embryos infected via the chorioallantoic membrane.

Chicks that hatch from eggs containing group specific antigen (gs antigen) of lymphoid leukosis virus (LLV) subgroups, grow poorly. In our laboratory for more precise identification of LLV-of subgroup A (LLV-A) resistant and susceptible genotypes by progeny testing, the chorioallantoic membrane (CAM) assay in complemented by liver tumour (LT) assay, wherein Rous sarcoma virus (RSV) of subgroup A (homologous to LLV-A) was used. The present study was conducted in a light breed (White Leghorn) and also in a heavy breed (Rhode Island Red) to ascertain the effect of infection on embryonic growth by RSV subgroup A. Mean relative body weight (rbw) of infected LT negative chicks of either breed exceeded the control highly significantly (P < 0.01) by 2%. However, neither the dose of virus inoculated per embryo, nor egg size influenced the relative body weight of day old chicks (P > 0.05). No difference in relative body weight of LT positive and control chicks was observed.

Expression of tumour phenotypes, hatchability and liver tumour mortality in two routes of inoculation in fowl.

A total of 350 and 200 eleven-day-olc embryos (pooled breeds) of twelve hatch replicates were inoculated with pseudotype of Bryan high titre, RSV(RAV-49) of subgroup C viz CAM (chorioallantoic membrane) and YS (yolk sac) route, respectively. An increase in hatchability (about 16%) and decrease in the incidence of CAM(+) [71%] and LT(+) [47%] phenotypes was noticed when inoculation was done via YS route as compared to the inoculation via CAM routes. A delay in LT(+) mortality was also recorded in YS route of infection. Chi-square analysis within a route basis indicated highly significant contingency (P < 0.01) in association of CAM infection phenotypes and LT incidence phenotypes for CAM route of infection in contrast to the YS route of infection.

Genetics of post-hatching survival potential of Australorp chicks infected as embryos by subgroup A Rous sarcoma virus: further support to 4-allele genetic model.

Embryos (II day-old) of Australorp breed were inoculated via chorioallantoic membrane (CAM) with subgroup A Rous sarcoma virus, and hatched subsequently. The post-hatch survival period in chicks was recorded upto the last chick that died by virus-induced liver tumour, which had a range from 3 to 50 days with an average of 13 +/- 8.7 days. The survival potential of progency tested Australorp parents selected on the basis of negative CAM-infection and those selected on uninoculated embryos, differed significantly (P less than 0.01) while maintaining an inverse relationship between liver tumour mortality and degrees of infection of CAMs. The homozygous susceptibles lacking either ar1 or ar2 or both alleles of the tva (tumour virus a) locus died within 7 days of post-hatching, supporting thereby 4-allele genetic model of tva locus recently proposed for the control of LT- and CAM-infection phenotypes.

Induced liver tumour deaths by subgroup A Rous sarcoma virus in chicks inoculated via chorioallantoic membrane, a genetic marker.

A study was made using two strains of light breed (White Leghorn strains, A and B) and four heavy beeds (Rhode Island Red, New Hampshire, Australorp, Columbian) to evaluate the breed difference in survival potential of chicks that were infected as 11-day-old embryos via chorioallantoic membranes (CAMs) with a subgroup A Rous sarcoma virus. Of the 1185 chicks hatched over multiple hatch-replicates, 845 chicks died rapidly of a fibrosarcomatous liver tumour (LT) with a peak mortality about 74% attained by the second week, post-hatch, in the heavy breeds and more than 90% by the second week in the light breed. The breeds did not differ in induced LT mortality when the chicks hatched from eggs that had at least 25 pock counts on CAMs, apparently genetically susceptible, i.e. 25 biologically active virus particles were enough to induce an unpreventable fatal LT. However, low pock-count on CAMs did not act as a pointer for predicting genetic resistance to infection because about 23% of chicks developed from eggs that had no pocks on CAMs, apparently genetically resistant, also died of LT, requiring further studies.