Developmental Regulation and Biological Functions of Root Border Cells in Higher Plants

Root border cells, previously referred to as sloughed root cap cells, is a special cell population which separates in large numbers from the periphery of the root cap and accumulates in the root tip. Recent evidence reveals that border cells, whose development is regulated by endogenous and exogenous signals, are biologically viable in the majority of higher plant species. As soon as border cells detach from root cap periphery, their metabolic activity dramatically increases in accordance with a differential gene expression from that in root cap cells. Recently, PsUGT1 and RCPME1, relevant to the early and late stage of border cell development, respectively, have been cloned and functionally identified. Border cells can synthesize specially and export a diverse array of chemicals including anthocyanins, antibiotics, special enzymes and other substances, that either inhibit or promote the growth of other entities in rhizosphere such as bacteria, fungi, viruses, and nematodes, and also antagonize some toxic chemicals around the root tip in soil such as aluminum toxicity. Therefore, there are multiple biological roles played by border cells during plant growth and development.

Developmental Characteristics and Cinnamic Acid Resistance of Root Border Cells in Cucumber and Figleaf Gourd Seedlings

Root border cells （RBCs） originate from the root tip epidermis and surround the root apices. In this study, we evaluated the developmental characteristics and the roles of RBCs in protection of root apices of cucumber and ifgleaf gourd seedlings from CA toxicity. The formation of RBCs and the emergence of the root tip occurred almost simultaneously in root apices of cucumber and ifgleaf gourd seedlings. CA ranging from 0 to 0.25 mol L-1 inhibited root elongation and decreased root cell viability in the root tip, moreover the inhibitory effects of CA were more signiifcant in the CA-sensitive cucumber than in the CA-tolerant ifgleaf gourd. Removal of RBCs from root tips led to more severe CA induced inhibition of root elongation and decline in root cell viability. Increasing CA levels and treatment time decreased the relative viability of attached and detached RBCs. CA also induced a thicker mucilage layer surrounding attached RBCs of both species. Additionally, a signiifcantly higher relative cell viability of attached RBCs and thicker mucilage layers were observed in ifgleaf gourd. These results suggest that RBCs play an important role in protecting root tips from CA toxicity.

Developmental characteristics and response to iron toxicity of root border cells in rice seedlings

To investigate the Fe^2＋ effects on root tips in rice plant, experiments were carried out using border cells in vitro. The border cells were pre-planted in aeroponic culture and detached from root tips. Most border cells have a long elliptical shape. The number and the viability of border cells in situ reached the maxima of 1600 and 97.5%, respectively, at 20---25 mm root length. This mortality was more pronounced at the first 1-12 h exposure to 250 mg/L Fe^2＋ than at the last 12-36 h. After 36 h, the cell viability exposed to 250 mg/L Fe^2＋ decreased to nought, whereas it was 46.5% at 0 mg/L Fe^2＋. Increased Fe^2＋ dosage stimulated the death of detached border cells from rice cultivars. After 4 h Fe^2＋ treatment, the cell viabilities were _〉80% at 0 and 50 mg/L Fe^2＋ treatment and were 〈62% at 150, 250 and 350 mg/L Fe^2＋ treatment; The viability of border cells decreased by 10% when the Fe^2＋ concentration increased by 100 mg/L. After 24 h Fe^2＋ treatment, the viabilities of border cells at all the Fe^2＋ levels were 〈65%; The viability of border cells decreased by 20% when the Fee＋ concentration increased by 100 mg/L. The decreased viabilities of border cells indicated that Fe^2＋ dosage and treatment time would cause deadly effect on the border cells. The increased cell death could protect the root tips from toxic harm. Therefore, it may protect root from the damage caused by harmful iron toxicity.

The leaf extract of crofton weed(Eupatorium adenophorum)inhibits primary root growth by inducing cell death in maize root border cells

The extract of crofton weed(Eupatorium adenophorum) inhibits seed germination and weed growth;however,the physiological mechanisms underlying the effect of crofton weed extract on the modulation of seedling growth and root system development remain largely unclear.In this study,we investigated the effects of the leaf extract of crofton weed(LECW) on primary root(PR) growth in maize seedlings.Treatment with LECW markedly inhibited seed germination and seedling growth in a dose-dependent manner.Physiological analysis indicated that the LECW induced reactive oxygen species(ROS) accumulation in root tips,thereby leading to cell swelling and deformation both in the root cap and elongation zone of root tips,finally leading to cell death in root border cells(RBCs) and PR growth inhibition.The LECW also inhibited pectin methyl esterase(PME) activity,thereby decreasing the RBC number.Taken together,our results indicated that the LECW inhibited PR growth by inducing ROS accumulation and subsequent cell death in RBCs.The present study provides a better understanding of how the LECW modifies root system development and provides insight for evaluating the toxicity of crofton weed extracts in plants.

In vivo RNAi screen identifies candidate signaling genes required for collective cell migration in Drosophila ovary

Collective migration of loosely or closely associated cell groups is prevalent in animal development, physiological events, and cancer metastasis. However, our understanding of the mechanisms of collective cell migration is incomplete. Drosophila border cells provide a powerful in vivo genetic model to study collective migration and identify essential genes for this process. Using border cell-specific RNAi-silencing in Drosophila, we knocked down 360 conserved signaling transduction genes in adult flies to identify essential pathways and genes for border cell migration. We uncovered a plethora of signaling genes, a large proportion of which had not been reported for border cells, including Rack1 （Receptor of activated C kinase） and brk （brinker）, mad （mother against dpp）, and sax （saxophone）, which encode three components of TGF-β signaling. The RNAi knock down phenotype was validated by clonal analysis of Rack1 mutants. Our data suggest that inhibition of Src activity by Rackl may be important for border cell migration and cluster cohesion maintenance. Lastly, results from our screen not only would shed light on signaling pathways involved in collective migration during embryogenesis and organogenesis in general, but also could help our understanding for the functions of conserved human genes involved in cancer metastasis.