Fruit development, not GPP, drives seasonal variation in NPP in a tropical palm plantation.

We monitored seasonal variations in net primary production (NPP), estimated by allometric equations from organ dimensions, gross primary production (GPP), estimated by the eddy covariance method, autotrophic respiration (R(a)), estimated by a model, and fruit production in a coconut (Cocos nucifera L.) plantation located in the sub-tropical South Pacific archipelago of Vanuatu. Net primary production of the vegetative compartments of the trees accumulated steadily throughout the year. Fruits accounted for 46% of tree NPP and showed large seasonal variations. On an annual basis, the sum of estimated NPP (16.1 Mg C ha(-1) year(-1)) and R(a) (24.0 Mg C ha(-1) year(-1)) for the ecosystem (coconut trees and herbaceous understory) closely matched GPP (39.0 Mg C ha(-1) year(-1)), suggesting adequate cross-validation of annual C budget methods. However, seasonal variations in NPP + R(a) were smaller than the seasonal variations in GPP, and maximum tree NPP occurred 6 months after the midsummer peak in GPP and solar radiation. We propose that this discrepancy reflects seasonal variation in the allocation of dry mass to carbon reserves and new plant tissue, thus affecting the allometric relationships used for estimating NPP.

Differential developmental regulation and functional effects on pre-TCR surface expression of human pTalpha(a) and pTalpha(b) spliced isoforms.

Functional rearrangement at the TCRbeta locus leads to surface expression on developing pre-T cells of a pre-TCR complex composed of the TCRbeta-chain paired with the invariant pre-TCRalpha (pTalpha) chain and associated with CD3 components. Pre-TCR signaling triggers the expansion and further differentiation of pre-T cells into TCRalphabeta mature T cells, a process known as beta selection. Besides the conventional pTalpha transcript (termed pTalpha(a)), a second, alternative spliced, isoform of the pTalpha gene (pTalpha(b)) has been described, whose developmental relevance remains unknown. In this study, phenotypic, biochemical, and functional evidence is provided that only pTalpha(a) is capable of inducing surface expression of a CD3-associated pre-TCR complex, which seems spontaneously recruited into lipid rafts, while pTalpha(b) pairs with and retains TCRbeta intracellularly. In addition, by using real-time quantitative RT-PCR approaches, we show that expression of pTalpha(a) and pTalpha(b) mRNA spliced products is differentially regulated along human intrathymic development, so that pTalpha(b) transcriptional onset is developmentally delayed, but beta selection results in simultaneous shutdown of both isoforms, with a relative increase of pTalpha(b) transcripts in beta-selected vs nonselected pre-T cells in vivo. Relative increase of pTalpha(b) is also shown to occur upon pre-T cell activation in vitro. Taken together, our data illustrate that transcriptional regulation of pTalpha limits developmental expression of human pre-TCR to intrathymic stages surrounding beta selection, and are compatible with a role for pTalpha(b) in forming an intracellular TCRbeta-pTalpha(b) complex that may be responsible for limiting surface expression of a pTalpha(a)-containing pre-TCR and/or may be competent to signal from a subcellular compartment.