The Arabidopsis genes AS1, AS2 and JAG negatively regulate boundary-specifying genes to promote sepal and petal development Export

@article{citeulike:2192228, abstract = {Boundary formation is crucial for organ development in multicellular eukaryotes. In higher plants, boundaries that separate the organ primordia from their surroundings have relatively low rates of cell proliferation. This cellular feature is regulated by the actions of certain boundary-specifying genes, whose ectopic expression in organs can cause inhibition of the organ growth. Here we show that the Arabidopsis ASYMMETRIC LEAVES1 and 2 (AS1 and AS2) and JAGGED (JAG) genes function in the sepal and petal primordia to repress boundary-specifying genes for normal development of the organs. Loss-of-function as1 jag and as2 jag double mutants produced extremely tiny sepals and petals. Analysis of a cell-cycle marker HISTONE 4 revealed that cell division in sepal primordia of the double mutant was inhibited. Moreover, these abnormal sepals and petals exhibited ectopic overexpression of the boundary-specifying genes PETAL LOSS (PTL), CUP-SHAPED COTYLEDONS1 and 2 (CUC1 and CUC2). Loss of PTL or CUC1 and CUC2 functions in the as1 jag background could partially rescue the tiny sepal and petal phenotypes, supporting the model that the tiny sepal/petal phenotypes are caused, at least in part, by ectopic expression of the boundary-specifying genes. Together, our data reveal a previously unrecognized fundamental regulation, by which AS1, AS2 and JAG act to define sepal and petal from their boundaries. 10.1104/pp.107.113787}, author = {Xu, Ben and Li, Ziyu and Zhu, Yan and Wang, Hua and Ma, Hong and Dong, Aiwu and Huang, Hai}, citeulike-article-id = {2192228}, citeulike-linkout-0 = {http://dx.doi.org/10.1104/pp.107.113787}, citeulike-linkout-1 = {http://view.ncbi.nlm.nih.gov/pubmed/18156293}, citeulike-linkout-2 = {http://www.hubmed.org/display.cgi?uids=18156293}, day = {21}, doi = {10.1104/pp.107.113787}, journal = {Plant Physiol.}, keywords = {as1, flower-development, lbd}, month = {December}, pages = {pp.107.113787+}, posted-at = {2008-01-03 20:33:33}, priority = {2}, title = {The Arabidopsis genes AS1, AS2 and JAG negatively regulate boundary-specifying genes to promote sepal and petal development}, url = {http://dx.doi.org/10.1104/pp.107.113787}, year = {2007} }

TY - JOUR ID - citeulike:2192228 L3 - citeulike-article-id:2192228 N2 - Boundary formation is crucial for organ development in multicellular eukaryotes. In higher plants, boundaries that separate the organ primordia from their surroundings have relatively low rates of cell proliferation. This cellular feature is regulated by the actions of certain boundary-specifying genes, whose ectopic expression in organs can cause inhibition of the organ growth. Here we show that the Arabidopsis ASYMMETRIC LEAVES1 and 2 (AS1 and AS2) and JAGGED (JAG) genes function in the sepal and petal primordia to repress boundary-specifying genes for normal development of the organs. Loss-of-function as1 jag and as2 jag double mutants produced extremely tiny sepals and petals. Analysis of a cell-cycle marker HISTONE 4 revealed that cell division in sepal primordia of the double mutant was inhibited. Moreover, these abnormal sepals and petals exhibited ectopic overexpression of the boundary-specifying genes PETAL LOSS (PTL), CUP-SHAPED COTYLEDONS1 and 2 (CUC1 and CUC2). Loss of PTL or CUC1 and CUC2 functions in the as1 jag background could partially rescue the tiny sepal and petal phenotypes, supporting the model that the tiny sepal/petal phenotypes are caused, at least in part, by ectopic expression of the boundary-specifying genes. Together, our data reveal a previously unrecognized fundamental regulation, by which AS1, AS2 and JAG act to define sepal and petal from their boundaries. 10.1104/pp.107.113787 JF - Plant Physiol. TI - The Arabidopsis genes AS1, AS2 and JAG negatively regulate boundary-specifying genes to promote sepal and petal development SP - pp.107.113787 KW - as1 KW - flower-development KW - lbd AU - Xu, Ben AU - Li, Ziyu AU - Zhu, Yan AU - Wang, Hua AU - Ma, Hong AU - Dong, Aiwu AU - Huang, Hai PY - 2007/12/21/ UR - http://dx.doi.org/10.1104/pp.107.113787 ER -