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Vulnerability segmentation (VS), an important mechanism for protecting plants from drought, hypothesizes that the distal organs of a plant should be more susceptible to embolism than the basal organs. However, experimental studies testing the VS hypothesis for trees are limited and have reached inconsistent conclusions. Here, we tested the VS hypothesis with three angiosperms and four conifers co-existing in a temperate forest in northeastern China. The results showed that the difference in vulnerability to cavitation between leaves and branches (P 50leaf–branch) was positive for the conifers but negative for the angiosperms, implying that the conifers rather than the angiosperms exhibited VS. The conifers had lower leaf hydraulic safety margins and more embolism-resistant branches than the angiosperms. Although the angiosperms did not display VS, they took a hydraulic compensatory strategy (e.g. great leaf and branch hydraulic conductivities) to maintain the water supply of their leaves. In addition, we found a significant trade-off between the sapwood-specific hydraulic conductivity (K SS) and xylem pressure inducing 50% loss of hydraulic conductivity (P 50branch) across all species. Both K SS and P 50branch increased with the area-based light-saturated photosynthetic rate (A area), suggesting that increased embolism resistance of branches comes at the cost of reduced hydraulic efficiency, which in turn constrains the photosynthesis. A area was negatively correlated with P 50leaf–branch, further indicating that the conifers had strong VS and were associated with a conservative strategy. Conversely, the angiosperms displayed an acquisitive strategy, tending to have higher A area, leaf and branch hydraulic conductivities, but lower embolism resistance. These differentiations in the functional traits between the angiosperms and conifers provide potential mechanisms for their co-existence in this temperate forest community. [ABSTRACT FROM AUTHOR]

Plant growth requires cell wall extension. The cotton AtRD22-Like 1 gene GhRDL1, predominately expressed in elongating fiber cells, encodes a BURP domain-containing protein. Here, we show that GhRDL1 is localized in cell wall and interacts with GhEXPA1, an α-expansin functioning in wall loosening. Transgenic cotton overexpressing GhRDL1 showed an increase in fiber length and seed mass, and an enlargement of endopleura cells of ovules. Expression of either GhRDL1 or GhEXPA1 alone in Arabidopsis led to a substantial increase in seed size; interestingly, their co-expression resulted in the increased number of siliques, the nearly doubled seed mass, and the enhanced biomass production. Cotton plants overexpressing GhRDL1 and GhEXPA1 proteins produced strikingly more fruits (bolls), leading to up to 40% higher fiber yield per plant without adverse effects on fiber quality and vegetative growth. We demonstrate that engineering cell wall protein partners has a great potential in promoting plant growth and crop yield. [ABSTRACT FROM PUBLISHER]

Phosphatidylinositol monophosphate 5-kinase (PIP5K) plays an essential role in coordinating plant growth, especially in response to environmental factors. To explore the physiological function of PIP5K, we characterized Arabidopsis thaliana PIP5K9, which is constitutively expressed. We found that a T-DNA insertion mutant, pip5k9-d, which showed enhanced PIP5K9 transcript levels, had shortened primary roots owing to reduced cell elongation. Transgenic plants overexpressing PIP5K9 displayed a similar root phenotype. Yeast two-hybrid assays identified a cytosolic invertase, CINV1, that interacted with PIP5K9, and the physiological relevance of this interaction was confirmed by coimmunoprecipitation studies using plant extracts. CINV1-deficient plants, cinv1, had reduced activities of both neutral and acid invertases as well as shortened roots. Invertase activities in pip5k9-d seedlings were also reduced, suggesting a negative regulation of CINV1 by PIP5K9. In vitro studies showed that PIP5K9 interaction indeed repressed CINV1 activities. Genome-wide expression studies revealed that genes involved in sugar metabolism and multiple developmental processes were altered in pip5k9-d and cinv1, and the altered sugar metabolism in these mutants was confirmed by metabolite profiling. Together, our results indicate that PIP5K9 interacts with CINV1 to negatively regulate sugar-mediated root cell elongation. [ABSTRACT FROM AUTHOR]