ABI3 affects plastid differentiation in dark-grown Arabidopsis seedlings

The Arabidopsis ABSCISIC ACID-INSENSITIVE3 (ABI3) protein has been identified previously as a crucial regulator of late seed development. Here, we show that dark-grown abi3 plants, or abi3 plants returned to the dark after germination in the light, developed and maintained an etioplast with a prominent prolamellar body at developmental stages in which the wild type did not. Overexpression of ABI3 led to the preservation of the plastid ultrastructure that was present at the onset of darkness. These observations suggest that ABI3 plays a role in plastid differentiation pathways in vegetative tissues. Furthermore, the analysis of deetiolated (det1) abi3 double mutants revealed that DET1 and ABI3 impinge on a multitude of common processes. During seed maturation, ABI3 required DET1 to achieve its full expression. Mature det1 abi3 seeds were found to be in a highly germinative state, indicating that germination is controlled by both DET1 and ABI3. During plastid differentiation in leaves of dark-grown plants, DET1 is required for the action of ABI3 as it is during seed development. Together, the results suggest that ABI3 is at least partly regulated by light.     

Developmental and environmental regulation of tissue- and cell-specific expression for a pea protein farnesyltransferase gene in transgenic plants

Farnesylation mediates membrane targeting and in vivo activities of several key regulatory proteins such as Ras and Ras-related GTPases and protein kinases in yeast and mammals, and is implicated in cell cycle control and abscisic acid (ABA) signaling in plants. In this study, the developmental expression of a pea protein farnesyl-transferase (FTase) gene was examined using transgenic expression of the β-glucuronidase (GUS) gene fused to a 3.2 kb 5′ upstream sequence of the gene encoding the pea FTase β subunit. Coordinate expression of the GUS transgene and endogenous tobacco FTase β subunit gene in tobacco cell lines suggests that the 3.2 kb region contains the key FTase promoter elements. In transgenic tobacco plants, GUS expression is most prominent in meristematic tissues such as root tips, lateral root primordia and the shoot apex, supporting a role for FTase in the control of the cell cycle in plants. GUS activity was also detected in mature embryos and imbibed embryos, in accordance with a role for FTase in ABA signaling that modulates seed dormancy and germination. In addition, GUS activity was detected in regions that border two organs, e.g. junctions between stems and leaf petioles, cotyledons and hypocotyls, roots and hypocotyls, and primary and secondary roots. GUS is expressed in phloem complexes that are adjacent to actively growing tissues such as young leaves, roots of light-grown seedlings, and hypocotyls of dark-grown seedlings. Both light and sugar (e.g. sucrose) treatments repressed GUS expression in dark-grown seedlings. These expression patterns suggest a potential involvement of FTase in the regulation of nutrient allocation into actively growing tissues.     

PtABI3 impinges on the growth and differentiation of embryonic leaves during bud set in poplar

The Arabidopsis ABSCISIC ACID-INSENSITIVE3 (ABI3) protein plays a crucial role during late seed development and has an additional function at the vegetative meristem, particularly during periods of growth-arresting conditions and quiescence. Here, we show that the ABI3 homolog of poplar (PtABI3) is expressed in buds during natural bud set. Expression occurs clearly after perception of the critical daylength that initiates bud set and dormancy in poplar. In short-day conditions mimicking natural bud set, the expression of a chimeric PtABI3::beta-glucuronidase (GUS) gene occurred in those organs and cells of the apex that grow actively but will undergo arrest: the young embryonic leaves, the subapical meristem, and the procambial strands. If PtABI3 is overexpressed or downregulated, bud development in short-day conditions is altered. Constitutive overexpression of PtABI3 resulted in apical buds with large embryonic leaves and small stipules, whereas in antisense lines, bud scales were large and leaves were small. Thus, PtABI3 influences the size and ratio of embryonic leaves and bud scales/stipules that differentiate from the primordia under short-day conditions. These observations, together with the expression of PtABI3::GUS in embryonic leaves but not in bud scales/stipules, support the idea that wild-type PtABI3 is required for the relative growth rate and differentiation of embryonic leaves inside the bud. These experiments reveal that ABI3 plays a role in the cellular differentiation of vegetative tissues, in addition to its function in seeds.     

The BHLH Transcriptional Factor PIF4 Competes with the R2R3-MYB Transcriptional Factor MYB75 to Fine-Tune Seeds Germination under High Glucose Stress

It is known that the high level of sugar including glucose suppresses seed germination through ABA signal. ABI5 is an essential component to mediate ABA-dependent seed germination inhibition, but underlying mechanism needs more investigation. Previous study demonstrated the PIF4 activated the expression of ABI5 to suppress seed germination in darkness. Here we reported that PIF4 also mediated the seed germination inhibition through ABI5 under high concentration of glucose treatment. Furthermore, we found that PIF4 interacted with PAP1, the central factor to control anthocyanin biosynthesis. Such interaction was confirmed in vitro and in planta. Biochemical and physiological analysis revealed that PAP1 bond the promoter of ABI5 to suppress its expression, thus enhanced seed germination under high concentration of glucose treatment. Specially, PAP1 competed with PIF4 to antagonize the activation of PIF4 on ABI5 expression, thus promoted seed germination under high glucose treatment. Given these, we uncover a novel role for PIF4 and PAP1 in controlling seed germination under high glucose treatment, and reveal their antagonistic mechanism by which coordinates ABI5 expression to control seed germination in response to the glucose signal.