Leaf Development

Tsukaya, Hirokazu

doi:10.1199/tab.0072

Cited by 91 publications

(89 citation statements)

References 141 publications

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“…By contrast, the auxin-resistant1 ( axr1 ) mutant has obviously smaller leaves, inflorescence stems, and floral organs, and anatomic examination shows that the reduced size of its leaf and stem is caused by a decrease in cell number rather than cell size (Lincoln et al, 1990). Although these observations suggest that AXR1 might be involved in auxin-dependent cell proliferation during development (Tsukaya, 2002), there is no molecular data to support this claim.…”

Section: Introductionmentioning

confidence: 99%

The Arabidopsis Auxin-Inducible Gene ARGOS Controls Lateral Organ Size

2003

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Section: Introductionmentioning

confidence: 99%

The Arabidopsis Auxin-Inducible Gene ARGOS Controls Lateral Organ Size

2003

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“…In spite of considerable efforts to reveal the genetic and molecular mechanisms underlying cell fate determination in leaves, our understanding is still largely limited (Tsukaya, 2002a;Tsukaya, 2002b;Tsukaya, 2002c). In this report, we describe the bop1-1 mutation that induces abnormal expression of class I knox genes.…”

mentioning

confidence: 97%

TheBLADE-ON-PETIOLE 1gene controls leaf pattern formation through the modulation of meristematic activity inArabidopsis

et al. 2003

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The plant leaf provides an ideal system to study the mechanisms of organ formation and morphogenesis. The key factors that control leaf morphogenesis include the timing, location and extent of meristematic activity during cell division and differentiation. We identified an Arabidopsis mutant in which the regulation of meristematic activities in leaves was aberrant. The recessive mutant allele blade-on-petiole1-1 (bop1-1)produced ectopic, lobed blades along the adaxial side of petioles of the cotyledon and rosette leaves. The ectopic organ, which has some of the characteristics of rosette leaf blades with formation of trichomes in a dorsoventrally dependent manner, was generated by prolonged and clustered cell division in the mutant petioles. Ectopic, lobed blades were also formed on the proximal part of cauline leaves that lacked a petiole. Thus, BOP1regulates the meristematic activity of leaf cells in a proximodistally dependent manner. Manifestation of the phenotypes in the mutant leaves was dependent on the leaf position. Thus, BOP1 controls leaf morphogenesis through control of the ectopic meristematic activity but within the context of the leaf proximodistality, dorsoventrality and heteroblasty.BOP1 appears to regulate meristematic activity in organs other than leaves, since the mutation also causes some ectopic outgrowths on stem surfaces and at the base of floral organs. Three class I knox genes,i.e., KNAT1, KNAT2 and KNAT6, were expressed aberrantly in the leaves of the bop1-1 mutant. Furthermore, the bop1-1 mutation showed some synergistic effect in double mutants with as1-1 oras2-2 mutation that is known to be defective in the regulation of meristematic activity and class I knox gene expression in leaves. Thebop1-1 mutation also showed a synergistic effect with thestm-1 mutation, a strong mutant allele of a class I knoxgene, STM. We, thus, suggest that BOP1 promotes or maintains a developmentally determinate state in leaf cells through the regulation of class I knox genes.

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“…Possibly, the presence of cotyledons is required during embryogenesis to define and organise the SAM properly (Torres Ruiz, 2004). This would be reminiscent of postembryonic development where genes expressed in the adaxial and abaxial sides of leaves are thought to influence SAM development (Siegfried et al, 1999;Sawa et al, 1999;McConnell et al, 2001;Kerstetter et al, 2001;Kumaran et al, 2002;Tsukaya, 2002). Double mutant combinations of cuc1, cuc2 and cuc3 genes, which develop one fused cotyledon and no SAM, suggested a requirement of bilateral symmetry and cotyledon boundaries for SAM formation (Aida et al, 1997;Aida et al, 1999;Vroemen et al, 2003).…”

Section: Mutations In Enhancer Of Pinoid and Pinoid Cause The Laternementioning

confidence: 99%

The geneENHANCER OF PINOIDcontrols cotyledon development in theArabidopsisembryo

et al. 2005

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During Arabidopsis embryo development, cotyledon primordia are generated at transition stage from precursor cells that are not derived from the embryonic shoot apical meristem (SAM). To date, it is not known which genes specifically instruct these precursor cells to elaborate cotyledons, nor is the role of auxin in cotyledon development clear. In laternemutants, the cotyledons are precisely deleted, yet the hypocotyl and root are unaffected. The laterne phenotype is caused by a combination of two mutations: one in the PINOID (PID) gene and another mutation in a novel locus designated ENHANCER OF PINOID (ENP). The expression domains of shoot apex organising genes such as SHOOT MERISTEMLESS (STM) extend along the entire apical region of laterne embryos. However, analysis of pid enp stm triple mutants shows that ectopic activity of STM does not appear to cause cotyledon obliteration. This is exclusively caused by enp in concert with pid. In pinoid embryos, reversal of polarity of the PIN1 auxin transport facilitator in the apex is only occasional, explaining irregular auxin maxima in the cotyledon tips. By contrast, polarity of PIN1:GFP is completely reversed to basal position in the epidermal layer of the laterne embryo. Consequently auxin, which is believed to be essential for organ formation, fails to accumulate in the apex. This strongly suggests that ENP specifically regulates cotyledon development through control of PIN1 polarity in concert with PID.

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Leaf Development

Cited by 91 publications

References 141 publications

The Arabidopsis Auxin-Inducible Gene ARGOS Controls Lateral Organ Size

The Arabidopsis Auxin-Inducible Gene ARGOS Controls Lateral Organ Size

TheBLADE-ON-PETIOLE 1gene controls leaf pattern formation through the modulation of meristematic activity inArabidopsis

The geneENHANCER OF PINOIDcontrols cotyledon development in theArabidopsisembryo

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