The Experts below are selected from a list of 108 Experts worldwide ranked by ideXlab platform

Jeff A. Long - One of the best experts on this subject based on the ideXlab platform.

  • Control of Arabidopsis apical–basal Embryo Polarity by antagonistic transcription factors
    Nature, 2010
    Co-Authors: Zachery R. Smith, Jeff A. Long
    Abstract:

    Plants, similarly to animals, form polarized axes during Embryogenesis on which cell differentiation and organ patterning programs are orchestrated. During Arabidopsis Embryogenesis, establishment of the shoot and root stem cell populations occurs at opposite ends of an apical–basal axis. Recent work has identified the PLETHORA ( PLT ) genes as master regulators of basal/root fate^ 1 , 2 , 3 , whereas the master regulators of apical/shoot fate have remained elusive. Here we show that the PLT1 and PLT2 genes are direct targets of the transcriptional co-repressor TOPLESS ( TPL ) and that PLT1/2 are necessary for the homeotic conversion of shoots to roots in tpl-1 mutants. Using tpl-1 as a genetic tool, we identify the CLASS III HOMEODOMAIN-LEUCINE ZIPPER ( HD-ZIP III ) transcription factors as master regulators of Embryonic apical fate, and show they are sufficient to drive the conversion of the Embryonic root pole into a second shoot pole. Furthermore, genetic and misexpression studies show an antagonistic relationship between the PLT and HD-ZIP III genes in specifying the root and shoot poles. During Embryogenesis in Arabidopsis , the shoot stem cell and root stem cell populations are established at the apical and basal pole, respectively. While, it is known that the PLETHORA genes function as master regulators of root fate, the regulators of shoot fate are unknown. Zachery Smith and Jeff Long now show that the Class III homeodomain-leucine zipper ( HD-ZIP III ) transcription factors are master regulators of Embryonic apical shoot fate, and that they are sufficient to drive the conversion of the Embryonic root pole into a second shoot pole. During development in Arabidopsis plants, populations of shoot stem cells and root stem cells are established at the Embryo's apical and basal poles, respectively. PLETHORA genes are master regulators of root fate, but the regulators of shoot fate were unknown. Here, CLASS III HOMEODOMAIN-LEUCINE ZIPPER genes are identified as master regulators of apical/shoot fate, and are shown to be sufficient to convert the Embryonic root pole into a second shoot pole.

  • control of arabidopsis apical basal Embryo Polarity by antagonistic transcription factors
    Nature, 2010
    Co-Authors: Zachery R. Smith, Jeff A. Long
    Abstract:

    During Embryogenesis in Arabidopsis, the shoot stem cell and root stem cell populations are established at the apical and basal pole, respectively. While, it is known that the PLETHORA genes function as master regulators of root fate, the regulators of shoot fate are unknown. Zachery Smith and Jeff Long now show that the Class III homeodomain-leucine zipper (HD-ZIP III) transcription factors are master regulators of Embryonic apical shoot fate, and that they are sufficient to drive the conversion of the Embryonic root pole into a second shoot pole. During development in Arabidopsis plants, populations of shoot stem cells and root stem cells are established at the Embryo's apical and basal poles, respectively. PLETHORA genes are master regulators of root fate, but the regulators of shoot fate were unknown. Here, CLASS III HOMEODOMAIN-LEUCINE ZIPPER genes are identified as master regulators of apical/shoot fate, and are shown to be sufficient to convert the Embryonic root pole into a second shoot pole. Plants, similarly to animals, form polarized axes during Embryogenesis on which cell differentiation and organ patterning programs are orchestrated. During Arabidopsis Embryogenesis, establishment of the shoot and root stem cell populations occurs at opposite ends of an apical–basal axis. Recent work has identified the PLETHORA (PLT) genes as master regulators of basal/root fate1,2,3, whereas the master regulators of apical/shoot fate have remained elusive. Here we show that the PLT1 and PLT2 genes are direct targets of the transcriptional co-repressor TOPLESS (TPL) and that PLT1/2 are necessary for the homeotic conversion of shoots to roots in tpl-1 mutants. Using tpl-1 as a genetic tool, we identify the CLASS III HOMEODOMAIN-LEUCINE ZIPPER (HD-ZIP III) transcription factors as master regulators of Embryonic apical fate, and show they are sufficient to drive the conversion of the Embryonic root pole into a second shoot pole. Furthermore, genetic and misexpression studies show an antagonistic relationship between the PLT and HD-ZIP III genes in specifying the root and shoot poles.

Zachery R. Smith - One of the best experts on this subject based on the ideXlab platform.

  • Control of Arabidopsis apical–basal Embryo Polarity by antagonistic transcription factors
    Nature, 2010
    Co-Authors: Zachery R. Smith, Jeff A. Long
    Abstract:

    Plants, similarly to animals, form polarized axes during Embryogenesis on which cell differentiation and organ patterning programs are orchestrated. During Arabidopsis Embryogenesis, establishment of the shoot and root stem cell populations occurs at opposite ends of an apical–basal axis. Recent work has identified the PLETHORA ( PLT ) genes as master regulators of basal/root fate^ 1 , 2 , 3 , whereas the master regulators of apical/shoot fate have remained elusive. Here we show that the PLT1 and PLT2 genes are direct targets of the transcriptional co-repressor TOPLESS ( TPL ) and that PLT1/2 are necessary for the homeotic conversion of shoots to roots in tpl-1 mutants. Using tpl-1 as a genetic tool, we identify the CLASS III HOMEODOMAIN-LEUCINE ZIPPER ( HD-ZIP III ) transcription factors as master regulators of Embryonic apical fate, and show they are sufficient to drive the conversion of the Embryonic root pole into a second shoot pole. Furthermore, genetic and misexpression studies show an antagonistic relationship between the PLT and HD-ZIP III genes in specifying the root and shoot poles. During Embryogenesis in Arabidopsis , the shoot stem cell and root stem cell populations are established at the apical and basal pole, respectively. While, it is known that the PLETHORA genes function as master regulators of root fate, the regulators of shoot fate are unknown. Zachery Smith and Jeff Long now show that the Class III homeodomain-leucine zipper ( HD-ZIP III ) transcription factors are master regulators of Embryonic apical shoot fate, and that they are sufficient to drive the conversion of the Embryonic root pole into a second shoot pole. During development in Arabidopsis plants, populations of shoot stem cells and root stem cells are established at the Embryo's apical and basal poles, respectively. PLETHORA genes are master regulators of root fate, but the regulators of shoot fate were unknown. Here, CLASS III HOMEODOMAIN-LEUCINE ZIPPER genes are identified as master regulators of apical/shoot fate, and are shown to be sufficient to convert the Embryonic root pole into a second shoot pole.

  • control of arabidopsis apical basal Embryo Polarity by antagonistic transcription factors
    Nature, 2010
    Co-Authors: Zachery R. Smith, Jeff A. Long
    Abstract:

    During Embryogenesis in Arabidopsis, the shoot stem cell and root stem cell populations are established at the apical and basal pole, respectively. While, it is known that the PLETHORA genes function as master regulators of root fate, the regulators of shoot fate are unknown. Zachery Smith and Jeff Long now show that the Class III homeodomain-leucine zipper (HD-ZIP III) transcription factors are master regulators of Embryonic apical shoot fate, and that they are sufficient to drive the conversion of the Embryonic root pole into a second shoot pole. During development in Arabidopsis plants, populations of shoot stem cells and root stem cells are established at the Embryo's apical and basal poles, respectively. PLETHORA genes are master regulators of root fate, but the regulators of shoot fate were unknown. Here, CLASS III HOMEODOMAIN-LEUCINE ZIPPER genes are identified as master regulators of apical/shoot fate, and are shown to be sufficient to convert the Embryonic root pole into a second shoot pole. Plants, similarly to animals, form polarized axes during Embryogenesis on which cell differentiation and organ patterning programs are orchestrated. During Arabidopsis Embryogenesis, establishment of the shoot and root stem cell populations occurs at opposite ends of an apical–basal axis. Recent work has identified the PLETHORA (PLT) genes as master regulators of basal/root fate1,2,3, whereas the master regulators of apical/shoot fate have remained elusive. Here we show that the PLT1 and PLT2 genes are direct targets of the transcriptional co-repressor TOPLESS (TPL) and that PLT1/2 are necessary for the homeotic conversion of shoots to roots in tpl-1 mutants. Using tpl-1 as a genetic tool, we identify the CLASS III HOMEODOMAIN-LEUCINE ZIPPER (HD-ZIP III) transcription factors as master regulators of Embryonic apical fate, and show they are sufficient to drive the conversion of the Embryonic root pole into a second shoot pole. Furthermore, genetic and misexpression studies show an antagonistic relationship between the PLT and HD-ZIP III genes in specifying the root and shoot poles.

Lynette A Scott - One of the best experts on this subject based on the ideXlab platform.

  • oocyte and Embryo Polarity
    Seminars in Reproductive Medicine, 2000
    Co-Authors: Lynette A Scott
    Abstract:

    The development of all low-order animals and noneutherian mammals follows an organized, polarized directional course from fertilization through fetal development. New evidence points to a fundamental polarization during all steps of mammalian development, from the early oocyte through fertilization and gastrulation. The generator of this polarization is primarily at the genetic level, with the results of gene expression and checkpoints being manifested in phenotype. Although cell-cell interactions reinforce the polarization of the Embryo, they are not the underlying means of establishing axes in eutherian Embryos. The ability of mammalian cells to remain totipotent is only partial, with little evidence that isolated blastomeres can result in full fetal development. The isolated blastomere can, however, contribute to development if reintroduced into a polarized environment. Polarization begins in the unovulated oocyte and is reinforced at fertilization. The axes and polarization established at fertilization endure through to the blastocyst stage and define the axes during gastrulation and fetal development.

Kenneth J. Kemphues - One of the best experts on this subject based on the ideXlab platform.

  • par 2 lgl 1 and the cdc 42 gap chin 1 act in distinct pathways to maintain Polarity in the c elegans Embryo
    Development, 2013
    Co-Authors: Alexander Beatty, Diane G. Morton, Kenneth J. Kemphues
    Abstract:

    In the one-cell C. elegans Embryo, Polarity is maintained by mutual antagonism between the anterior cortical proteins PAR-3, PKC-3, PAR-6 and CDC-42, and the posterior cortical proteins PAR-2 and LGL-1 on the posterior cortex. The mechanisms by which these proteins interact to maintain Polarity are incompletely understood. In this study, we investigate the interplay among PAR-2, LGL-1, myosin, the anterior PAR proteins and CDC-42. We find that PAR-2 and LGL-1 affect cortical myosin accumulation by different mechanisms. LGL-1 does not directly antagonize the accumulation of cortical myosin and instead plays a role in regulating PAR-6 levels. By contrast, PAR-2 likely has separate roles in regulating cortical myosin accumulation and preventing the expansion of the anterior cortical domain. We also provide evidence that asymmetry of active CDC-42 can be maintained independently of LGL-1 and PAR-2 by a redundant pathway that includes the CDC-42 GAP CHIN-1. Finally, we show that, in addition to its primary role in regulating the size of the anterior cortical domain via its binding to PAR-6, CDC-42 has a secondary role in regulating cortical myosin that is not dependent on PAR-6.

  • A Genome-wide RNAi Screen for Enhancers of Par Mutants Reveals New Contributors to Early Embryonic Polarity in Caenorhabditis elegans
    Genetics, 2012
    Co-Authors: Diane G. Morton, Wendy A. Hoose, Kenneth J. Kemphues
    Abstract:

    The par genes of Caenorhabditis elegans are essential for establishment and maintenance of early Embryo Polarity and their homologs in other organisms are crucial Polarity regulators in diverse cell types. Forward genetic screens and simple RNAi depletion screens have identified additional conserved regulators of Polarity in C. elegans; genes with redundant functions, however, will be missed by these approaches. To identify such genes, we have performed a genome-wide RNAi screen for enhancers of lethality in conditional par-1 and par-4 mutants. We have identified 18 genes for which depletion is synthetically lethal with par-1 or par-4, or both, but produces little Embryo lethality in wild type. Fifteen of the 18 genes identified in our screen are not previously known to function in C. elegans Embryo Polarity and 11 of them also increase lethality in a par-2 mutant. Among the strongest synthetic lethal genes, Polarity defects are more apparent in par-2 early Embryos than in par-1 or par-4, except for strd-1(RNAi), which enhances early Polarity phenotypes in all three mutants. One strong enhancer of par-1 and par-2 lethality, F25B5.2, corresponds to nop-1, a regulator of actomyosin contractility for which the molecular identity was previously unknown. Other putative Polarity enhancers identified in our screen encode cytoskeletal and membrane proteins, kinases, chaperones, and sumoylation and deubiquitylation proteins. Further studies of these genes should give mechanistic insight into pathways regulating establishment and maintenance of cell Polarity.

Alexander Beatty - One of the best experts on this subject based on the ideXlab platform.

  • par 2 lgl 1 and the cdc 42 gap chin 1 act in distinct pathways to maintain Polarity in the c elegans Embryo
    Development, 2013
    Co-Authors: Alexander Beatty, Diane G. Morton, Kenneth J. Kemphues
    Abstract:

    In the one-cell C. elegans Embryo, Polarity is maintained by mutual antagonism between the anterior cortical proteins PAR-3, PKC-3, PAR-6 and CDC-42, and the posterior cortical proteins PAR-2 and LGL-1 on the posterior cortex. The mechanisms by which these proteins interact to maintain Polarity are incompletely understood. In this study, we investigate the interplay among PAR-2, LGL-1, myosin, the anterior PAR proteins and CDC-42. We find that PAR-2 and LGL-1 affect cortical myosin accumulation by different mechanisms. LGL-1 does not directly antagonize the accumulation of cortical myosin and instead plays a role in regulating PAR-6 levels. By contrast, PAR-2 likely has separate roles in regulating cortical myosin accumulation and preventing the expansion of the anterior cortical domain. We also provide evidence that asymmetry of active CDC-42 can be maintained independently of LGL-1 and PAR-2 by a redundant pathway that includes the CDC-42 GAP CHIN-1. Finally, we show that, in addition to its primary role in regulating the size of the anterior cortical domain via its binding to PAR-6, CDC-42 has a secondary role in regulating cortical myosin that is not dependent on PAR-6.