EMB30 is essential for normal cell division, cell expansion, and cell adhesion in Arabidopsis and encodes a protein that has similarity to Sec7

Shevell, Diane E.; Leu, Wei Ming; Gillmor, C. Stewart; Xia, Gui-Xian; Feldmann, Kenneth A.; Chua, Nam Hai

doi:10.1016/0092-8674(94)90444-8

Cited by 296 publications

(221 citation statements)

References 51 publications

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“…Additional functional data also suggest that interactions between Arf and the FG loop of ArfGEF are indeed important in vivo. Mutation of ArfGEF E97 to lysine results in the emb30 mutant of Arabidopsis (Shevell et al, 1994), and in yeast, the ArfGETs GEA1 and GEA2 were identified as high- copy suppressors of the semidominant cold-sensitive mutations arf2-G29A and arf2-T31N, which lie to either side of K30 (arf1-105) (Peyroche et al, 1996). The binding partner of Arf1 R99 (arf1-114), SEC7 Q99, is also important for catalytic activity, because mutation of this residue results in a 90% loss of exchange activity relative to wild-type protein (Mossessova et al, 1998).…”

Section: Mutations In Proposed Arfgef-binding Site Of Arf1pmentioning

confidence: 99%

Systematic Structure-Function Analysis of the Small GTPase Arf1 in Yeast

Click¹,

Stearns

Botstein³

2002

MBoC

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Members of the ADP-ribosylation factor (Arf) family of small GTPases are implicated in vesicle traffic in the secretory pathway, although their precise function remains unclear. We generated a series of 23 clustered charge-to-alanine mutations in the Arf1 protein ofSaccharomyces cerevisiae to determine the portions of this protein important for its function in cells. These mutants display a number of phenotypes, including conditional lethality at high or low temperature, defects in glycosylation of invertase, dominant lethality, fluoride sensitivity, and synthetic lethality with thearf2 null mutation. All mutations were mapped onto the available crystal structures for Arf1p: Arf1p bound to GDP, to GTP, and complexed with the regulatory proteins ArfGEF and ArfGAP. From this systematic structure-function analysis we demonstrate that all essential mutations studied map to one hemisphere of the protein and provide strong evidence in support of the proposed ArfGEF contact site on Arf1p but minimal evidence in support of the proposed ArfGAP-binding site. In addition, we describe the isolation of a spatially distant intragenic suppressor of a dominant lethal mutation in the guanine nucleotide-binding region of Arf1p.

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Section: Mutations In Proposed Arfgef-binding Site Of Arf1pmentioning

confidence: 99%

Systematic Structure-Function Analysis of the Small GTPase Arf1 in Yeast

Click¹,

Stearns

Botstein³

2002

MBoC

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“…The strong gnom alleles emb30-1 and xg33 named 'gnom' in the following were used as the mutant background for both marker analysis and transactivation of GNOM (Shevell et al, 1994;Busch et al, 1996). Because the marker/promotor expression pattern in gnom did not always match with the expression pattern in wild type, each of the transactivator lines was carefully analyzed in gnom before the rescue analysis was performed.…”

Section: Plant Materialsmentioning

confidence: 99%

Coordination of apical and basal embryo development revealed by tissue-specific GNOM functions

et al. 2011

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SUMMARYFlowering-plant embryogenesis generates the basic body organization, including the apical and basal stem cell niches, i.e. shoot and root meristems, the major tissue layers and the cotyledon(s). gnom mutant embryos fail to initiate the root meristem at the early-globular stage and the cotyledon primordia at the late globular/transition stage. Tissue-specific GNOM expression in the gnom mutant embryo revealed that both apical and basal embryo organization depend on GNOM provascular expression and a functioning apical-basal auxin flux: GNOM provascular expression in gnom mutant background resulted in non-cell-autonomous reconstitution of apical and basal tissues which could be linked to changes in auxin responses in those tissues, stressing the importance of apical-basal auxin flow for overall embryo organization. Although reconstitution of apical-basal auxin flux in gnom results in the formation of single cotyledons (monocots), only additional GNOM epidermal expression is able to induce wild-type apical patterning. We conclude that provascular expression of GNOM is vital for both apical and basal tissue organization, and that epidermal GNOM expression is required for radial-to-bilateral symmetry transition of the embryo. We propose GNOM-dependent auxin sinks as a means to generate auxin gradients across tissues.

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“…Thus, a future goal is to identify proteins that interact with, or act in the same pathway as, the RHD3 protein. Potential candidates include the products of genes defined by cell expansion mutant phenotypes (Schiefelbein and Somerville 1990;Benfey et al 1993;Shevell et al 1994;Aeschbacher et al 1995;Hauser et al 1995;Takahashi et al 1995) and genes defined by rhd3 suppresser mutations. The ease with which cell enlargement can be analyzed in the developing Arabidopsis root epidermis should continue to be an advantage in further studies of the RHD3 pathway.…”

Section: Rhds-hke Proteins May Participate In a Fundamental Eukaryotimentioning

confidence: 99%

The ROOT HAIR DEFECTIVE3 gene encodes an evolutionarily conserved protein with GTP-binding motifs and is required for regulated cell enlargement in Arabidopsis.

Wang¹,

Lockwood²,

Hoeltzel³

et al. 1997

Genes Dev.

152

153

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In plants, morphogenesis is largely determined by the orientation and extent of cell enlargement. To define the molecular mechanisms regulating plant cell enlargement, we have conducted a molecular genetic analysis of the ROOT HAIR DEFECTIVES [RHDS) gene of Arabidopsis thaliana. Mutations affecting the RHD3 gene were found to alter cell size, but not cell number, in tissues throughout the plant. Genetic and physiological analyses suggest that the RHD3 gene is not required for proper cell type specification, and it is likely to act downstream of the hormones auxin and ethylene. The RHD3 gene was cloned by a T-DNA tagging method and confirmed by the molecular complementation of the rhd3 mutant phenotype and by the analyses of six rhdS mutant alleles. Consistent with the global effects of the rhd3 mutations, the RHD3 gene is expressed in all major plant organs. The deduced RHDS product is a novel 89-kD polypeptide with putative GTP-binding motifs near the amino terminus. i?iiD3-like genes were identified from a protozoan {Entamoeba histolytica), a fungus {Saccharomyces cerevisiae), and another plant species {Oryza sativa), with the sequence identity including the putative GTP-binding motifs. These results imply that the RHDS protein is a member of a new class of GTP-binding proteins that is widespread in eukaryotes and required for regulated cell enlargement.

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EMB30 is essential for normal cell division, cell expansion, and cell adhesion in Arabidopsis and encodes a protein that has similarity to Sec7

Cited by 296 publications

References 51 publications

Systematic Structure-Function Analysis of the Small GTPase Arf1 in Yeast

Systematic Structure-Function Analysis of the Small GTPase Arf1 in Yeast

Coordination of apical and basal embryo development revealed by tissue-specific GNOM functions

The ROOT HAIR DEFECTIVE3 gene encodes an evolutionarily conserved protein with GTP-binding motifs and is required for regulated cell enlargement in Arabidopsis.

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