Os03g0706500 - Revision history

192.168.72.52: /* Structured Information */

2015-06-12T05:58:40Z

‎Structured Information

Huanghs: /* background */

2014-06-03T04:58:52Z

‎background

Huanghs at 04:27, 3 June 2014

2014-06-03T04:27:23Z

Huanghs at 04:26, 3 June 2014

2014-06-03T04:26:21Z

Gaojin: /* References */

2014-06-02T17:57:43Z

‎References

Gaojin: /* background */

2014-06-02T17:54:36Z

‎background

Gaojin: /* References */

2014-06-02T17:50:04Z

‎References

Gaojin: /* Annotated Information */

2014-06-02T17:49:16Z

‎Annotated Information

Gaojin: /* References */

2014-05-30T04:49:25Z

‎References

Gaojin: /* Knowledge Extension */

2014-05-30T04:46:50Z

‎Knowledge Extension

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 ==Structured Information==
 [[Category:Genes]]
 [[Category:Japonica mRNA]]

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 ==Annotated Information==
-=== background ===
+=== Background ===
 Plant architecture is determined by the pattern of shoot branching <ref name="McSteen and Leyser 2005" />. In most higher plants, shoot branches develop from axillary buds in the axils of leaves. Not all of the axillary buds develop, and each is subjected to a decision to continue growth or to become dormant, depending on a complex interplay between environmental and endogenous cues. Plant hormones are major players in the control of axillary bud growth. It has been known for a long time that two hormones in particular, auxin and cytokinin, are involved in this control. Auxin, which is supplied from the apical bud, indirectly suppresses axillary bud outgrowth, while cytokinins directly induce branching. During the past two decades, genetic and physiological analyses in pea and Arabidopsis have predicted the involvement of an additional, novel hormone in the control of shoot branching (for reviews, see<ref name="Beveridge 2006" /><ref name="Ongaro and Leyser 2008" /> . Recently it was demonstrated that the novel hormone, which inhibits bud outgrowth, is the group of compounds called strigolactones (SLs) or their downstream metabolites <ref name="Gomez-Roldan et al. 2008" /><ref name="Umehara et al. 2008" />.
 Prior to the discovery of SLs as the branching hormone, more axillary growth1 (max1) to max4in Arabidopsis and five ramosus (rms) mutants in garden pea ( Pisum sativum)  had been identifi ed as components of a novel graft-transmissible branching signal pathway <ref name="Strinberg et al. 2002" /><ref name="Sorefan et al. 2003" />.Consistent with results obtained from grafting experiments, max1 max3 and max4 were shown to be SL deficient, and their defects were rescued by the external application of an SL<ref name="Gomez-Roldan et al. 2008" /><ref name="Umehara et al. 2008" />. On the other hand, a mutant of the MAX2 gene, which encodes an F-box leucine-rich repeat (LRR)-containing protein, was not rescued by the SL <ref name="Strinberg et al. 2002" />. MAX1 encodes CYP711A1, a class III cytochrome P450 <ref name="Booker et al. 2005" />. MAX3 and MAX4 encode carotenoid cleavage dioxygenases (CCDs) <ref name="Sorefan et al. 2003" /><ref name="Booker et al. 2004" />.
 The SL pathway seems to be well conserved across species <ref name="Beveridge and Kyozuka 2010"/>. Molecular cloning showed that pea RMS1,   RMS4and RMS5are orthologs of MAX4,   MAX2 and MAX3, respectively <ref name="Sorefan et al. 2003" /><ref name="Foo et al. 2005" /><ref name="Jhonson et al. 2006" /><ref name="Beveridge et al. 2009" />. Analyses of branching mutants in rice indicated that the pathway is also conserved in monocot species. We reported on five tillering dwarf mutants of rice, dwarf3 (d3),  d10,   d14,   d17 and d27<ref name="Ishikawa et al. 2005" />. The high tillering dwarf1 (htd1) mutant, which resembles the five d mutants, was also described <ref name="Zou et al. 2006" />. After the molecular cloning, it turned out that D3and D10are orthologs of MAX2/RMS4and MAX4/RMS1, respectively <ref name="Ishikawa et al. 2005" /><ref name="Arite et al. 2007" />, while HTD1 encodes an ortholog of MAX3/RMS5, and is the same locus as D17<ref name="Zou et al. 2006" /><ref name="Umehara et al. 2008" />. Meanwhile, D14and D27were shown to be novel genes that work in the SL pathway <ref name="Arite et al. 2009" /><ref name="Lin et al. 2009" />. D27 encodes an iron-containing protein and is likely to be involved in SL biosynthesis <ref name="Lin et al. 2009" />. The d14mutant, also reported as d88and htd2, is insensitive to exogenous SL application and contains elevated SL levels <ref name="Arite et al. 2009" /><ref name="Gao et al. 2009" /><ref name="Liu et al. 2009" />. Although its molecular function has not yet been determined, it is postulated that D14also works in SL signaling <ref name="Arite et al. 2009" />.
 The mechanisms controlling cross-talk between the hormones are beginning to be elucidated. Recently it was revealed that one role of auxin is to suppress cytokinin biosynthesis in the stem <ref name="Tanaka et al. 2006" /><ref name="Shimizu-Sato et al. 2009" />. When the auxin supply from the apical bud is blocked, expression of isopentenyltransferase ( IPT) genes, which encode a rate-limiting enzyme of cytokinin biosynthesis, is rapidly up-regulated, and this results in the rapid synthesis of cytokinins in the stem. This cytokinin is transported to axillary buds and induces bud outgrowth. In addition, the auxin-dependent up-regulation of SL biosynthesis genes has been observed in all plant species analyzed so far <ref name="Arite et al. 2007" /><ref name="Heyward et al. 2009" />. Although actual changes in SL levels have not yet been observed, a likely scenario is that the apically derived auxin induces SL biosynthesis, and the SLs act as second messengers to inhibit axillary bud outgrowth. Furthermore, SL biosynthesis is controlled by feedback regulation <ref name="Arite et al. 2007" /><ref name="Heyward et al. 2009" /> and, at least in Arabidopsis, this feedback regulation is mostly dependent on auxin signaling<ref name="Heyward et al. 2009" />. Together, these observations suggest that the growth of axillary buds is controlled by multiple independent and interacting pathways <ref name="Dun et al. 2009" />.
 Despite the remarkable progress in our understanding of the frameworks that control axillary bud outgrowth, little is known so far about how SLs act to control shoot branching. As a fi rst step towards understanding SL action at the molecular level, we report here that rice FINE CULM1 (FC1) partially works downstream of SLs to inhibit bud outgrowth. We propose that FC1serves as a hub gene where multiple signals are integrated to fi ne-tune the development of axillary  buds.
 ===Function===

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 ==Annotated Information==
-== background ==
+=== background ===
 Plant architecture is determined by the pattern of shoot branching <ref name="McSteen and Leyser 2005" />. In most higher plants, shoot branches develop from axillary buds in the axils of leaves. Not all of the axillary buds develop, and each is subjected to a decision to continue growth or to become dormant, depending on a complex interplay between environmental and endogenous cues. Plant hormones are major players in the control of axillary bud growth. It has been known for a long time that two hormones in particular, auxin and cytokinin, are involved in this control. Auxin, which is supplied from the apical bud, indirectly suppresses axillary bud outgrowth, while cytokinins directly induce branching. During the past two decades, genetic and physiological analyses in pea and Arabidopsis have predicted the involvement of an additional, novel hormone in the control of shoot branching (for reviews, see<ref name="Beveridge 2006" /><ref name="Ongaro and Leyser 2008" /> . Recently it was demonstrated that the novel hormone, which inhibits bud outgrowth, is the group of compounds called strigolactones (SLs) or their downstream metabolites <ref name="Gomez-Roldan et al. 2008" /><ref name="Umehara et al. 2008" />.
 Prior to the discovery of SLs as the branching hormone, more axillary growth1 (max1) to max4in Arabidopsis and five ramosus (rms) mutants in garden pea ( Pisum sativum)  had been identifi ed as components of a novel graft-transmissible branching signal pathway <ref name="Strinberg et al. 2002" /><ref name="Sorefan et al. 2003" />.Consistent with results obtained from grafting experiments, max1 max3 and max4 were shown to be SL deficient, and their defects were rescued by the external application of an SL<ref name="Gomez-Roldan et al. 2008" /><ref name="Umehara et al. 2008" />. On the other hand, a mutant of the MAX2 gene, which encodes an F-box leucine-rich repeat (LRR)-containing protein, was not rescued by the SL <ref name="Strinberg et al. 2002" />. MAX1 encodes CYP711A1, a class III cytochrome P450 <ref name="Booker et al. 2005" />. MAX3 and MAX4 encode carotenoid cleavage dioxygenases (CCDs) <ref name="Sorefan et al. 2003" /><ref name="Booker et al. 2004" />.

← Older revision		Revision as of 04:26, 3 June 2014
Line 1:		Line 1:
−	~~Please input one-sentence summary here.~~

	The OsTB1 gene, also known as FC1, encodes a protein which is a member of TCP gene family.The protein play a negative role in regulating tillering of rice.		The OsTB1 gene, also known as FC1, encodes a protein which is a member of TCP gene family.The protein play a negative role in regulating tillering of rice.

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 ==References==
 <references>
 <ref name="Arite et al. 2007">Arite ,  T. ,  Iwata ,  H. ,  Ohshima ,  K. ,  Maekawa ,  M. ,  Nakajima ,  M. ,  Kojima ,  M. , et  al .  ( 2007 )  DWARF10, an  RMS1/MAX4/DAD1ortholog, controls lateral bud outgrowth in rice . Plant J. 51 :  1019 – 1029 . </ref>
@@ Line 66: / Line 67: @@
 <ref name="McSteen and Leyser 2005">McSteen ,  P.  and  Leyser ,  O.  ( 2005 )  Shoot  branching .  Annu. Rev. Plant Biol. 56 :  353 – 374 . </ref>
 <ref name="Ongaro and Leyser 2008">Ongaro ,  V.  and  Leyser ,  O.  ( 2008 )  Hormonal  control  of  shoot  branching . J. Exp. Bot. 59 :  67 – 74 .</ref>
-<ref name="ref1">Shimizu-Sato ,  T. ,  Tanaka ,  M.  and  Mori ,  H.  ( 2009 )  Auxin–cytokinin interactions in the control of shoot branching . Plant Mol. Biol. 6 9 : 429 – 435 . </ref>
+<ref name="Shimizu-Sato et al. 2009">Shimizu-Sato ,  T. ,  Tanaka ,  M.  and  Mori ,  H.  ( 2009 )  Auxin–cytokinin interactions in the control of shoot branching . Plant Mol. Biol. 6 9 : 429 – 435 . </ref>
 <ref name="Sorefan et al. 2003">Sorefan ,  K. ,  Booker ,  J. ,  Haurogne ,  K. ,  Goussot ,  M. ,  Bainbridge ,  K. ,  Foo ,  E. , et  al .  ( 2003 )  MAX4and RMS1are orthologous dioxygenase-like genes that regulate shoot branching in Arabidopsis and pea . Genes Dev. 17 :  1469 – 1474 . </ref>
 <ref name="Strinberg et al. 2002">Stirnberg ,  P. ,  van  de  Sande ,  K.  and  Leyser ,  H.M.O.  ( 2002 )  MAX1 and MAX2control shoot lateral branching in Arabidopsis . Development 129 :  1131 – 1141 .</ref>
-<ref name="ref1">Tanaka ,  M. ,  Takei ,  K. ,  Kojima ,  M. ,  Sakakibara ,  H.  and  Mori ,  H.  ( 2006 ) Auxin controls local cytokinin biosynthesis in the nodal stem in apical  dominance .  Plant J. 45 :  1028 – 36 . </ref>
+<ref name="Tanaka et al. 2006">Tanaka ,  M. ,  Takei ,  K. ,  Kojima ,  M. ,  Sakakibara ,  H.  and  Mori ,  H.  ( 2006 ) Auxin controls local cytokinin biosynthesis in the nodal stem in apical  dominance .  Plant J. 45 :  1028 – 36 . </ref>
 <ref name="Umehara et al. 2008">Umehara ,  M. ,  Hanada ,  A. ,  Yoshida ,  S. ,  Akiyama ,  K. ,  Arite ,  T. , Takeda-Kamiya ,  N. ,  et  al .  ( 2008 )  Inhibition  of  shoot  branching  by new terpenoid plant hormones . Nature 455 :  195 – 200 . </ref>
 <ref name="Zou et al. 2006">Zou ,  J. ,  Zhang ,  S. ,  Zhang ,  W. ,  Li ,  G. ,  Chen ,  Z. ,  Zhai ,  W. ,  et  al .  ( 2006 )  The rice HIGH-TILLERING DWARF1encoding an ortholog of Arabidopsis MAX3is required for negative regulation of the outgrowth of axillary buds .  Plant J. 48 :  687 – 698 . </ref>

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 <ref name="李家洋nature12870">	Jiang L, Liu X, Xiong G, et al. DWARF 53 acts as a repressor of strigolactone signalling in rice[J]. Nature 2013.</ref>
 </references>
 ==Structured Information==
 {{JaponicaGene|

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 [[File:SLs signal patyway.jpg‎|right|thumb|150px|''A proposed model of Strigolactone(SL) signalling patyway <ref name="李家洋nature12870" />).'']]
 Strigolactones (SLs) are a group of newly identified plant hormones that control plant shoot branching<ref name="李家洋nature12870" />. SL signaling requires the hormone-dependent interaction of DWARF14 (D14) which is regulated by the interaction of OsMADS57 with OsTB1<ref name="NATURE rice-1" />.
-In this study, we have identified theD53gene that encodes a substrate of the SCF(D3) ubiquitination complex, and revealed that D53 functions as a repressor ofSL signalling. These results allow us to establish a model of SL signalling that is centred around a D14–D3–D53 signalling axis . In the presence of SLs, perception of SL by D14 and the SCF(D3) complex leads to ubiquitination of D53 and its subsequent degradation by the ubiquitin proteasome system, which in turn releases the repression of downstream target genes . In the d53 plant, the mutated D53 protein is resistant to ubiquitination and degradation, leading to the accumulation of d53, which blocks SL signalling and results in dwarf and high tillering phenotypes. The signalling paradigm of SLs is still emerging as SLs are a relatively new class of plant hormone for which many knowledge gaps still exist. Identification ofD53 as a repressor of SL signalling adds a critical piece of information that helps to paint the whole picture of the SL signalling pathways.
+In this study<ref name="李家洋nature12870" />, they have identified theD53gene that encodes a substrate of the SCF(D3) ubiquitination complex, and revealed that D53 functions as a repressor ofSL signalling. These results allow to establish a model of SL signalling that is centred around a D14–D3–D53 signalling axis . In the presence of SLs, perception of SL by D14 and the SCF(D3) complex leads to ubiquitination of D53 and its subsequent degradation by the ubiquitin proteasome system, which in turn releases the repression of downstream target genes . In the d53 plant, the mutated D53 protein is resistant to ubiquitination and degradation, leading to the accumulation of d53, which blocks SL signalling and results in dwarf and high tillering phenotypes. The signalling paradigm of SLs is still emerging as SLs are a relatively new class of plant hormone for which many knowledge gaps still exist. Identification ofD53 as a repressor of SL signalling adds a critical piece of information that helps to paint the whole picture of the SL signalling pathways.
-Moreover, our work has also provided an important paradigm for understanding signalling pathways of other plant hormones, for example, karrikins, a class of plant growth regulators found in the smoke of burning plants. Karrikin signalling involves MAX2 and KAI2, a D14-like a/b-hydrolase. It is probable that a similar protein to D53 could serve as the repressor of karrikin signalling. Indeed, multiple D53-like proteins are found in rice and inArabidopsis. We propose that these proteins could serve as repressors of signalling by karrikin and other plant hormones, in a similar way to D53 in SL signalling.<ref name="李家洋nature12870" />
+Moreover, the work has also provided an important paradigm for understanding signalling pathways of other plant hormones, for example, karrikins, a class of plant growth regulators found in the smoke of burning plants. Karrikin signalling involves MAX2 and KAI2, a D14-like a/b-hydrolase. It is probable that a similar protein to D53 could serve as the repressor of karrikin signalling. Indeed, multiple D53-like proteins are found in rice and inArabidopsis. We propose that these proteins could serve as repressors of signalling by karrikin and other plant hormones, in a similar way to D53 in SL signalling.<ref name="李家洋nature12870" />
 ==Labs working on this gene==