A mutation that allows endosperm development without fertilization.

Ohad, Nir; Margossian, Linda; Hsu, Yung-Chao; Williams, Chad M.; Repetti, Peter P.; Fischer, Robert L.

doi:10.1073/pnas.93.11.5319

Cited by 367 publications

(371 citation statements)

References 28 publications

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“…The Pc-G complex FERTILIZATION INDEPENDENT SEED (FIS) contains the SET domain protein MEDEA (MEA) [11], the VEFS domain protein FIS2 [12], and the WD40 domain protein FERTILIZA-TION INDEPENDENT ENDOSPERM (FIE) [13]. Loss-of-function mutations of FIS genes cause autonomous onset of cell division in the central cell in the absence of fertilization [14,15]. The FIS complex also includes the WD40 protein MULTICOPY SUPPRESSOR OF IRA 1 (MSI1) [16,17].…”

Section: Control Of Cell Cycle Progression Before and After Fertilizamentioning

confidence: 99%

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Endosperm: an integrator of seed growth and development

Berger

Grini

Schnittger

2006

Current Opinion in Plant Biology

167

107

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Section: Control Of Cell Cycle Progression Before and After Fertilizamentioning

confidence: 99%

“…The paternal allele of MEA and FIS2 is silenced. As a consequence, the maternal inheritance of a null allele, mea or fis2, cannot be rescued by a paternal wildtype MEA or FIS2 allele and is sufficient to cause maternal effects on endosperm development [11,14,15,17].…”

Section: Coordination Of Maternal and Zygotic Cues During Seed Develomentioning

confidence: 99%

Endosperm: an integrator of seed growth and development

Berger

Grini

Schnittger

2006

Current Opinion in Plant Biology

167

107

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“…Loss-of-function mutations in the FERTILIZATION-INDE-PENDENT ENDOSPERM ( FIE ) gene allow diploid endosperm development in the absence of fertilization (Ohad et al, 1996Chaudhury et al, 1997). This phenotype suggests that the wild-type FIE gene functions to suppress endosperm development until fertilization occurs.…”

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confidence: 99%

“…FIE is related to polycomb proteins from Drosophila ( EXTRA SEX COMBS [ ESC ;Gutjahr et al, 1995;Sathe and Harte, 1995]), mammals ( EM-BRYONIC ECTODERM DEVELOPMENT [ EED ;Schumacher et al, 1996;Sewalt et al, 1998]), and Caenorhabditis ( MA-TERNAL EFFECT STERILE6 [ MES6 ; Korf et al, 1998]). Drosophila ESC and mammalian EED promote interactions with other polycomb proteins that repress gene transcription at specific sites within the genome (Wall et al, 1995;Sondek et al, 1996;Ng et al, 1997).After fertilization, mutations in the FIE gene cause parentof-origin effects on seed development (Ohad et al, 1996;Chaudhury et al, 1997). For example, when a heterozygous fie/FIE plant is pollinated with wild-type pollen, half of the seed inherit a maternal mutant fie allele and subsequently abort their development, even in the presence of the wildtype paternal allele.…”

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confidence: 99%

Mutations in the FIE and MEA Genes That Encode Interacting Polycomb Proteins Cause Parent-of-Origin Effects on Seed Development by Distinct Mechanisms

et al. 2000

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In flowering plants, two cells are fertilized in the haploid female gametophyte. Egg and sperm nuclei fuse to form the embryo. A second sperm nucleus fuses with the central cell nucleus, which replicates to generate the endosperm, a tissue that supports embryo development. The FERTILIZATION-INDEPENDENT ENDOSPERM ( FIE ) and MEDEA ( MEA ) genes encode WD and SET domain polycomb proteins, respectively. In the absence of fertilization, a female gametophyte with a loss-of-function fie or mea allele initiates endosperm development without fertilization. fie and mea mutations also cause parent-of-origin effects, in which the wild-type maternal allele is essential and the paternal allele is dispensable for seed viability. Here, we show that FIE and MEA polycomb proteins interact physically, suggesting that the molecular partnership of WD and SET domain polycomb proteins has been conserved during the evolution of flowering plants. The overlapping expression patterns of FIE and MEA are consistent with their suppression of gene transcription and endosperm development in the central cell as well as their control of seed development after fertilization. Although FIE and MEA interact, differences in maternal versus paternal patterns of expression, as well as the effect of a recessive mutation in the DECREASE IN DNA METHYLATION1 ( DDM1 ) gene on mutant allele transmission, indicate that fie and mea mutations cause parent-of-origin effects on seed development by distinct mechanisms. INTRODUCTIONFlowering plant reproduction involves fertilization of two cells (reviewed in van Went and Willemse, 1984). Within the Arabidopsis ovule, the female gametophyte consists of an egg cell and two synergid cells at the micropylar end, a central cell in the middle, and three antipodal cells at the chalazal end. All are haploid except for the central cell, which contains two polar nuclei that fuse to form a diploid nucleus. Reproduction is initiated when an entering pollen tube discharges two genetically identical haploid sperm cells. Fertilization of the egg generates the diploid embryo, which passes through morphologically defined stages (globular, heart, torpedo, walking stick, early maturation, and maturation) (Goldberg et al., 1994;Jurgens and Mayer, 1994). During embryo development, two organ systems (axis and cotyledon) and three tissue layers (protoderm, procambium, and ground meristem) are specified (Lindsey and Topping, 1993;Jurgens, 1994;Meinke, 1994).Fertilization of the central cell generates the triploid endosperm, for which the pattern of development differs dramatically from that of the embryo. Arabidopsis endosperm development is characteristic of nuclear endosperm development in angiosperms (Mansfield and Briarty, 1990a;Webb and Gunning, 1991;Berger, 1999;Brown et al., 1999). The Arabidopsis primary endosperm nucleus replicates without cytokinesis to form a syncytium of nuclear-cytoplasmic domains that migrate to the periphery of the expanding central cell (Brown et al., 1999). When the embryo is at the globular/heart transi...

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“…The first to fourth true leaves of 21-d-old plants of the rfc3-1 mutant and the wild type were collected separately in Eppendorf tubes and treated with a chloral hydrate:glycerol:water solution (8:1:2) to clear the cells (Ohad et al, 1996). The epidermal cells on both the abaxial and adaxial leaf surfaces were photographed with a Zeiss Axiovert 200M microscope with an Axiocam HRm digital camera that permits visualization of optical sections within the leaf.…”

Section: Leaf Epidermal Cell and Root Cortex Cell Examinationmentioning

confidence: 99%

Negative Regulation of Systemic Acquired Resistance by Replication Factor C Subunit3 in Arabidopsis

et al. 2009

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Systemic acquired resistance (SAR) is a plant immune response induced by local necrotizing pathogen infections. Expression of SAR in Arabidopsis (Arabidopsis thaliana) plants correlates with accumulation of salicylic acid (SA) and up-regulation of Pathogenesis-Related (PR) genes. SA is an essential and sufficient signal for SAR. In a genetic screen to search for negative regulators of PR gene expression and SAR, we found a new mutant that is hypersensitive to SA and exhibits enhanced induction of PR genes and resistance against the virulent oomycete Hyaloperonospora arabidopsidis Noco2. The enhanced pathogen resistance in the mutant is Nonexpressor of PR genes1 independent. The mutant gene was identified by map-based cloning, and it encodes a protein with high homology to Replication Factor C Subunit3 (RFC3) of yeast and other eukaryotes; thus, the mutant was named rfc3-1. rfc3-1 mutant plants are smaller than wild-type plants and have narrower leaves and petals. On the epidermis of true leaves, there are fewer cells in rfc3-1 compared with the wild type. Cell production rate is reduced in rfc3-1 mutant roots, indicating that the mutated RFC3 slows down cell proliferation. As Replication Factor C is involved in replication-coupled chromatin assembly, our data suggest that chromatin assembly and remodeling may play important roles in the negative control of PR gene expression and SAR.

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A mutation that allows endosperm development without fertilization.

Cited by 367 publications

References 28 publications

Endosperm: an integrator of seed growth and development

Endosperm: an integrator of seed growth and development

Mutations in the FIE and MEA Genes That Encode Interacting Polycomb Proteins Cause Parent-of-Origin Effects on Seed Development by Distinct Mechanisms

Negative Regulation of Systemic Acquired Resistance by Replication Factor C Subunit3 in Arabidopsis

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