World wheat grain yields increased substantially in the 1960s and 1970s because farmers rapidly adopted the new varieties and cultivation methods of the so-called 'green revolution'. The new varieties are shorter, increase grain yield at the expense of straw biomass, and are more resistant to damage by wind and rain. These wheats are short because they respond abnormally to the plant growth hormone gibberellin. This reduced response to gibberellin is conferred by mutant dwarfing alleles at one of two Reduced height-1 (Rht-B1 and Rht-D1) loci. Here we show that Rht-B1/Rht-D1 and maize dwarf-8 (d8) are orthologues of the Arabidopsis Gibberellin Insensitive (GAI) gene. These genes encode proteins that resemble nuclear transcription factors and contain an SH2-like domain, indicating that phosphotyrosine may participate in gibberellin signalling. Six different orthologous dwarfing mutant alleles encode proteins that are altered in a conserved amino-terminal gibberellin signalling domain. Transgenic rice plants containing a mutant GAI allele give reduced responses to gibberellin and are dwarfed, indicating that mutant GAI orthologues could be used to increase yield in a wide range of crop species.

Plants live in fixed locations and survive adversity by integrating growth responses to diverse environmental signals. Here, we show that the nuclear-localized growth-repressing DELLA proteins of Arabidopsis integrate responses to independent hormonal and environmental signals of adverse conditions. The growth restraint conferred by DELLA proteins is beneficial and promotes survival. We propose that DELLAs permit flexible and appropriate modulation of plant growth in response to changes in natural environments.

The germination of Arabidopsis seeds is promoted by gibberellin (GA). Arabidopsis GAI, and RGA are genes encoding key GA signal-transduction components (GAI and RGA) that mediate GA regulation of stem elongation. The Arabidopsis genome contains two further genes, RGL1 and RGL2, that encode proteins (RGL1 and RGL2) that are closely related to GAI and RGA. Here, we show that RGL2 regulates seed germination in response to GA, and that RGL1, GAI, and RGA do not. In addition, we show that RGL2 transcript levels rise rapidly following seed imbibition, and then decline rapidly as germination proceeds. In situ GUS staining revealed that RGL2 expression in imbibed seeds is restricted to elongating regions of pre-emergent and recently emerged radicles. These observations indicate that RGL2 is a negative regulator of GA responses that acts specifically to control seed germination rather than stem elongation. Furthermore, as RGL2 expression is imbibition inducible, RGL2 may function as an integrator of environmental and endogenous cues to control seed germination.

The phytohormone gibberellin (GA) regulates the development and fertility of Arabidopsis flowers. The mature flowers of GA-deficient mutant plants typically exhibit reduced elongation growth of petals and stamens. In addition, GA-deficiency blocks anther development, resulting in male sterility. Previous analyses have shown that GA promotes the elongation of plant organs by opposing the function of the DELLA proteins, a family of nuclear growth repressors. However, it was not clear that the DELLA proteins are involved in the GA-regulation of stamen and anther development. We show that GA regulates cell elongation rather than cell division during Arabidopsis stamen filament elongation. In addition, GA regulates the cellular developmental pathway of anthers leading from microspore to mature pollen grain. Genetic analysis shows that the Arabidopsis DELLA proteins RGA and RGL2 jointly repress petal, stamen and anther development in GA-deficient plants, and that this function is enhanced by RGL1 activity. GA thus promotes Arabidopsis petal, stamen and anther development by opposing the function of the DELLA proteins RGA, RGL1 and RGL2.

Precise coordination between stamen and pistil development is essential to make a fertile flower. Mutations impairing stamen filament elongation, pollen maturation, or anther dehiscence will cause male sterility. Deficiency in plant hormone gibberellin (GA) causes male sterility due to accumulation of DELLA proteins, and GA triggers DELLA degradation to promote stamen development. Deficiency in plant hormone jasmonate (JA) also causes male sterility. However, little is known about the relationship between GA and JA in controlling stamen development. Here, we show that MYB21, MYB24, and MYB57 are GA-dependent stamen-enriched genes. Loss-of-function of two DELLAs RGA and RGL2 restores the expression of these three MYB genes together with restoration of stamen filament growth in GA-deficient plants. Genetic analysis showed that the myb21-t1 myb24-t1 myb57-t1 triple mutant confers a short stamen phenotype leading to male sterility. Further genetic and molecular studies demonstrate that GA suppresses DELLAs to mobilize the expression of the key JA biosynthesis gene DAD1, and this is consistent with the observation that the JA content in the young flower buds of the GA-deficient quadruple mutant ga1-3 gai-t6 rga-t2 rgl1-1 is much lower than that in the WT. We conclude that GA promotes JA biosynthesis to control the expression of MYB21, MYB24, and MYB57. Therefore, we have established a hierarchical relationship between GA and JA in that modulation of JA pathway by GA is one of the prerequisites for GA to regulate the normal stamen development in Arabidopsis.

Severe Arabidopsis (Arabidopsis thaliana) gibberellin (GA)-deficient mutant ga1-3 fails to germinate and is impaired in floral organ development. In contrast, the ga1-3 gai-t6 rga-t2 rgl1-1 rgl2-1 mutant confers GA-independent seed germination and floral development. This fact suggests that GA-regulated transcriptomes for seed germination and floral development are DELLA dependent. However, it is currently not known if all GA-regulated genes are GA regulated in a DELLA-dependent fashion and if a similar set of DELLA-regulated genes is mobilized to repress both seed germination and floral development. Here, we compared the global gene expression patterns in the imbibed seeds and unopened flower buds of the ga1-3 mutant with that of the wild type and of the ga1-3 gai-t6 rga-t2 rgl1-1 rgl2-1 mutant. We found that about one-half of total GA-regulated genes are apparently regulated in a DELLA-dependent fashion, suggesting that there might be a DELLA-independent or -partially-dependent component of GA-dependent gene regulation. A cross-comparison based on gene identity revealed that the GA-regulated DELLA-dependent transcriptomes in the imbibed seeds and flower buds are distinct from each other. Detailed ontology analysis showed that, on one hand, DELLAs differentially regulate the expression of different individual members of a gene family to run similar biochemical pathways in seeds and flower. Meanwhile, DELLAs control many functionally different genes to run specific pathways in seeds or flower buds to mark the two different developmental processes. Our data shown here not only confirm many previous reports but also single out some novel aspects of DELLA functions that are instructive to our future research.

Phytochrome is a family of photoreceptors that regulates plant photomorphogenesis; the best-characterized member of this family is phytochrome A. Here, we report the identification of novel mutations at three Arabidopsis loci (fhy1, fhy2, and fhy3) that confer an elongated hypocotyl in far-red but not in white light. fhy2 mutants are phytochrome A deficient, have reduced or undetectable levels of PHYA transcripts, and contain structural alterations within the PHYA gene. When grown in white light, fhy2 mutants are morphologically indistinguishable from wild-type plants. Thus, phytochrome A appears to be dispensable in white light-grown Arabidopsis plants. fhy2 alleles confer partially dominant phenotypes in far-red light, suggesting that the relative abundance of phytochrome A can affect the extent of the far-red-mediated hypocotyl growth inhibition response. Plants homozygous for the recessive fhy1 and fhy3 mutations have normal levels of functional phytochrome A. The FHY1 and FHY3 gene products may be responsible for the transduction of the far-red light signal from phytochrome A to downstream processes involved in hypocotyl growth regulation.

Transcription factor p53 forms a network with associated factors to regulate the cell cycle and apoptosis in response to environmental stresses. However, there is currently no direct genetic evidence to show if or how the p53 pathway functions during organogenesis. Here we present evidence to show that the zebrafish def (digestive-organ expansion factor) gene encodes a novel pan-endoderm-specific factor. A loss-of-function mutation in def confers hypoplastic digestive organs and selectively up-regulates the expression of ⌬113p53, counterpart to a newly identified isoform of p53 produced by an alternative internal promoter in intron 4 of the p53 gene in human. The increased ⌬113p53 expression is limited to within the mutant digestive organs, and this increase selectively induces the expression of p53-responsive genes to trigger the arrest of the cell cycle but not apoptosis, resulting in compromised organ growth in the mutant. Our data demonstrate that, while induction of expression of p53 and/or its isoforms is crucial to suppress abnormal cell growth, ⌬113p53 is tightly regulated by an organ/tissue-specific factor Def, especially during organogenesis, to prevent adverse inhibition of organ/tissue growth.[Keywords: Def (digestive-organ expansion factor); endoderm organogenesis; p53; zebrafish] Supplemental material is available at http://www.genesdev.org.