Abstract: In 2002, a workshop on Arabidopsis research in China was held in Shanghai, when a small group of Chinese plant scientists was working on this model species. Since then, we have witnessed the rapid growth of Arabidopsis research in China. This special issue of Journal of Integrative Plant Biology is dedicated exclusively to the Fourth Workshop on Arabidopsis Research in China, scheduled on November 30, 2005, in Beijing. In addition to reports collected in this special issue, the Chinese Arabidopsis community has been able to make significant contributions to many research fields. Here, I briefly summarize recent advances in Arabidopsis research in China. Fatty acid homeostasis has long been thought as an important mechanism to regulate cellular signaling in a variety of organisms, but little is known about the direct physiological consequence of this regulation in higher plants. The characterization of the MOD1 gene demonstrated that de novo fatty acid synthesis is fundamental for plant growth and development by regulating various cellular signaling activities, such as apoptosis. The MOD1 gene encodes an enoyl-acyl carrier protein reductase, which is a subunit of the fatty acid synthase complex. The mod1 mutation causes premature cell death and a variety of developmental defects (Mou et al. 2000). Analogously, a loss-of-function mutation in the PEAMT gene, which encodes a rate-limiting enzyme involved in an early step of membrane phospholipid phosphatidylcholine biosynthesis, causes a pleiotropic phenotype and temperature-sensitive male sterility, as well as hypersensitivity to salinity, highlighting the importance of this class of complex lipids in plant cellular signaling (Mou et al. 2002). In efforts to elucidate the molecular mechanism of leaf development, ERECTA was defined to act in the ASYMMETRIC LEAVES1 (AS1)-AS2 pathway, in which AS1 and AS2 may form a complex (Xu et al. 2003). Surprisingly, AS1and AS2 act synergistically with the RNA-dependent RNA polymerase RDR6 to repress BREVIPEDICELLUS (BP) and MicroRNA165/166 (miRNA165/166), which likely target class III HD-ZIP proteins (Li et al. 2005). Therefore, this highly interactive network plays a key role in specifying leaf adaxial identity. A systematic characterization of BP function is also reported in this issue (Wang et al. 2006). The WUSCHEL (WUS) gene is well known as a key component of shoot meristem development. A gain-of-function mutation in WUS causes the formation of ectopic floral buds along inflorescence stems, thus revealing a novel function of the homeodomain protein in floral meristem development (Xu et al. 2005). During reproductive development, the SLOW WALKER1 (SWA1) gene, encoding a WD40 protein involved in rRNA biogenesis, was found to be essential for the cell cycle progression during gametogenesis. The swa1 mutation causes asynchronous development of megagametophytes, leading to the developmental arrest of embryo sacs at various stages. In addition, SWA1 also appears to play a role in root development (Shi et al. 2005). Genome-wide identification and characterization of Arabidopsis S-locus F-box-like (AtSFL) genes have shed light on the molecular functions of these Antirrhinum orthologs in plant growth and development. It is interesting to note that mutations in several AtSFL genes cause defective embryogenesis or female gametogenesis (Wang et al. 2004). De novo synthesis of the phytohormone auxin has been thought to be primarily through a tryptophan (Trp)-dependent pathway. However, a Trp-independent pathway was identified and characterized, in which indole-3-glycerol phosphate appears to act as a branch-point compound in this novel pathway (Ouyang et al. 2000). More recently, an indole-3-acetic acid (IAA) carboxyl methyltransferase (IAMT1) was shown to convert IAA into methyl-IAA ester, thereby regulating auxin homeostasis. A gain-of-function mutation in IAMT1 causes dramatic hyponastic leaf phenotypes, consistent with a decreased expression level of several TCP genes that are known to regulate leaf curvature (Qin et al. 2005). In auxin signaling, the BUD1/MAPKK7 gene was characterized as a negative regulator of polar auxin transport and the gain-of-function mutant bud1 displays pleiotropic phenotype characteristics of the auxin-deficient syndrome (Dai et al. 2006). This study provides the first line of evidence showing the involvement of the conserved mitogen-activated protein kinase signaling cascade in the control of auxin signal transduction. In parallel with these findings, Auxin Response Factor (ARF) 10 and ARF16, two key regulators controlling root cap development, were found to be targeted by miRNA160. Overexpression of miRNA160 displays a phenotype similar to that of an arf10/arf16 double mutant, characteristics of uncontrolled cell divisions and blocked cell differentiation in the root distal region, thereby causing the formation of a tumor-like root apex and the loss of gravity sensing. Interestingly, the repression of ARF10 and ARF16 by miRNA160 appears to be auxin independent (Wang et al. 2005). Previous genetic and molecular studies indicate that auxin-mediated lateral root development requires multiple components, such as the transcription factor NAC1 and an F-box protein TIR1. However, two recent studies suggest that the regulatory network is more complicated than expected. Overexpression of the novel transcription factor gene NAC2 promotes the formation of lateral roots, a phenotype similar to that of NAC1. In contrast with NAC1, NAC2 is regulated by auxin, ethylene, and abscisic acid (ABA), as well as by salt stress. Moreover, the salt regulation of NAC2 requires functional auxin and ethylene pathways, although its physiological significance remains unclear. It was proposed that NAC2 functions in regulating lateral root development by the integration of environmental and endogenous stimuli (He et al. 2005). A second new player in lateral root development is the auxin-inducible gene CEGENDUO (CEG), which encodes a novel F-box protein. The formation of lateral roots is promoted in a ceg-knockout mutant, but inhibited in transgenic plants overexpressing CEG. Therefore, CEG appears to negatively regulate lateral root formation in an auxin-dependent manner (Dong et al. 2006). Although polar transport of auxin has been well documented, very little is known about the transport of other plant hormones. Equilibrative nucleoside transporters (ENTs) are a class of evolutionarily conserved proteins that are involved in the transport of nucleosides in all eukaryotic organisms. Molecular and biochemical studies identified eight ENT genes in the Arabidopsis genome (Li et al. 2003). A recent study suggests that AtENT8/SOI33 and AtENT3 appear to function as transporters of cytokinin, a phytohormone derived from nucleosides (Sun et al. 2005). Equally exciting findings were also made in studies on brassinosteroid signaling. Brassinosteroids have long been appreciated as key regulators of cell elongation. However, brassinosteroids were also found to be important for cell division in a CycD3-dependent manner (Hu et al. 2000). Moreover, brassinosteroids were found not only to alter the expression of PIN genes, which encode auxin efflux carrier proteins, but also to promote functional localization of PIN2 modulated by ROP. Consistent with these observations, brassinosteroids were manifested to promote plant tropisms by modulating polar auxin transport (Li et al. 2005). Remarkably, a novel membrane steroid-binding protein (MSBP1) was found to be capable of binding various steroids, including 24-epi-brassinolide, in an in vitro assay. Transgenic studies suggest that the MSBP1 expression level is well correlated with the steroid-binding capacity, reduced cell elongation, and shorter hypocotyls, as well as sensitivities to exogenous progesterone and 24-epi-brassinolide. Thus, the light-responsive MSBP1 acts as a negative regulator of steroid signaling by controlling cell elongation and hypocotyl elongation (Yang et al. 2005). This study identifies the first functional steroid-binding protein in higher plants. Cryptochrome1 (CRY1) is a blue light receptor that mediates light signaling, presumably through its C-terminal domain. In an effort to characterize the N-terminal domain of CRY1 functionally, Sang et al. (2005) revealed that this domain was essential for dimerization of the photoreceptor, which, in turn, was required for light activation of the C-terminal domain. Intriguingly, CRY1 and CRY2 were also shown to be involved in the control of stomatal opening, which is physiologically connected to both water evaporation and photosynthesis in plants (Mao et al. 2005). Calcium has been implied in many aspects of cellular signaling in plants. The PPF1 gene, encoding a putative calcium ion carrier, is functional in both plant and human cells. The PPF1 gene appears to play an important role in multiple signaling pathways, particularly in the control of the flowering time. Indeed, whereas overexpression of PPF1 caused a late flowering phenotype, suppression of PPF1 expression resulted in an opposite phenotype (Wang et al. 2003). On the other hand, biochemical and physiological studies have demonstrated the presence of the Ca2+-permeable channels in the plasma membranes of pollens and pollen tubes. Moreover, dynamic actin microfilaments have been shown to control Ca2+ channel activity, which may, consequently, regulate cytoplasmic Ca2+, thus playing crucial roles in the regulation of pollen germination and tube growth (Wang et al. 2004). Cytosolic free Ca2+ in the regulation of stomatal movement has also been documented. Extracellular calmodulin was found to induce an increased level of H2O2 and cytosolic free Ca2+, leading to a reduction in stomatal aperture. Genetic analysis indicates that the extracellular calmodulin-modulated intracellular signaling is involved in the activation of a heterotrimeric G-protein (Chen et al. 2004). Epigenetic control of plant growth and development has been emerging as a main theme in recent years. In addition to the functional characterization of several microRNAs highlighted above, two recent studies have provided important insights into the epigenetic regulation in Arabidopsis. In root development, the identity of epidermal cells is determined by a small group patterning genes. Hyperacetylation of the core histones H3 and H4, manipulated by trichostatin A (TSA; an inhibitor of histone deacetylase) treatment or a mutation in a histone deacetylase gene, altered the expression of these patterning genes, thereby causing misspecified identity of certain epidermal cells (Xu et al. 2005). In a genetic screen for suppressors of ros1, which causes transcriptional silencing of a transgene and a homologous endogenous gene (Gong et al. 2002), two allelic mutants, namely ror1-1 and ror1-2, were identified. The ROR1 gene, encoding a protein similar to DNA replication protein A2, is involved in epigenetic gene silencing, likely in a DNA methylation-independent manner (Xia et al. 2006). In efforts in functional genomics programs, an ORFeome collection, representing 1 282 Arabidopsis transcription factor (TF) genes, was generated. Using a 70-mer-oligo array, the expression profiles of 66 MADS-box transcription factor genes and the relative distribution of expression abundance of 858 transcription factors were analyzed (Gong et al. 2004). A database of Arabidopsis transcription factors (DATF), representing 1 826 TF genes from 56 families, has been established at Peking University (Guo et al. 2005; see also http://datf.cbi.pku.edu.cn). Among these TF genes, two families, AP2/EREBP (Feng et al. 2005) and MYB (Chen et al. 2005), have been analyzed systematically and intensively. In addition, more than 125 000 T-DNA activation tagging lines were generated. These lines were generated using a 35S enhancer vector (PKU lines; 85 000 lines) and a chemical-inducible vector (IGDB lines; 40 000 lines), of which approximate 30 000 lines have been released to academic users (Qin et al. 2003; Zhang et al. 2005). Whereas these tremendous efforts and impressive achievements have been made during the past few years at a remarkably encouraging pace, the Arabidopsis research community keeps growing and becoming stronger in China. Therefore, we have every reason to believe in a great future for this young and energetic community. Acknowledgements I am grateful to Drs Jia-Yang Li, Yong-Biao Xue, Kang Chong, Hong-Wei Xue, Wei-Cai Yang and Jian-Ru Zuo for critically reading the manuscript. I would apologize to colleagues whose work is not cited in this minireview owing to space limitations.(Author for correspondence.College of Life Sciences, Peking University, Beijing 100871, China.Tel: +86 (0)10 6275 1200; Fax: +86 (0)10 6275 1207; E-mail: xuzh@pku.edu.cn)