Os05g0154700 - Revision history

192.168.72.52: /* Structured Information */

2015-06-12T07:30:20Z

‎Structured Information

Xu Congli: /* Labs working on this gene */

2014-06-06T01:09:54Z

‎Labs working on this gene

Xu Congli: /* Labs working on this gene */

2014-06-06T01:06:42Z

‎Labs working on this gene

Xu Congli: /* References */

2014-06-06T00:54:28Z

‎References

Xu Congli: /* Evolution */

2014-06-05T16:38:49Z

‎Evolution

Show changes

Xu Congli: /* Evolution */

2014-06-05T16:36:43Z

‎Evolution

Xu Congli: /* References */

2014-06-05T16:35:25Z

‎References

Xu Congli: /* Labs working on this gene */

2014-06-05T16:33:16Z

‎Labs working on this gene

Xu Congli: /* Function */

2014-06-05T16:30:42Z

‎Function

Xu Congli: /* References */

2014-06-05T16:19:18Z

‎References

@@ Line 124: / Line 124: @@
 ==Structured Information==
 [[Category:Genes]]
 [[Category:Japonica mRNA]]

← Older revision		Revision as of 01:09, 6 June 2014
Line 83:		Line 83:

	SIBS-UC Berkeley		SIBS-UC Berkeley
−
−	~~BioCassava Plus~~
−	~~International Potato Center~~
−	~~IITA~~
−	~~CIAT~~
−	~~Cornell University Cassava Database~~

	Institute of plant physiology & ecology, Shanghai institutes for biological sciences,CAS		Institute of plant physiology & ecology, Shanghai institutes for biological sciences,CAS

@@ Line 78: / Line 78: @@
 PCP Article Award
 PCP Annual Cover Contes
 ==References==

@@ Line 100: / Line 100: @@
 Fujisawa Y, Kato T, Ohki S, Ishikawa A, Kitano H, Sasaki T, et al. Suppression of the heterotrimeric G protein causes abnomal morphology, including dwarfism, in rice. Proc. Natl Acad. Sci. USA 1999;96:7575-7580.
   Guo L, Ho CM, Kong Z, Lee YR, Qian Q, Liu B. Evaluating the microtubule cytoskeleton and its interacting proteins in monocots by mining the rice genome. Ann. Bot. 2009;103:387-402.
 ==Structured Information==

← Older revision		Revision as of 16:36, 5 June 2014
Line 38:		Line 38:

	The causal gene of a novel small and round seed mutant phenotype (srs3) in rice was identified by map-based cloning and named the SRS3 gene. The SRS3 gene was grouped as a member of the kinesin 13 subfamily. The SRS3 gene codes for a protein of 819 amino acids that contains a kinesin motor domain and a coiled-coil structure. Using scanning electron microscopy, we determined that the cell length of seeds in the longitudinal direction in srs3 is shorter than that in the wild type. The number of cells of seeds in the longitudinal direction in srs3 was not very different from that in the wild type. The result suggests that the small and round seed phenotype of srs3 is due to a reduction in cell length of seeds in the longitudinal direction. The SRS3 protein, which is found in the crude microsomal fraction, is highly expressed in developing organs.		The causal gene of a novel small and round seed mutant phenotype (srs3) in rice was identified by map-based cloning and named the SRS3 gene. The SRS3 gene was grouped as a member of the kinesin 13 subfamily. The SRS3 gene codes for a protein of 819 amino acids that contains a kinesin motor domain and a coiled-coil structure. Using scanning electron microscopy, we determined that the cell length of seeds in the longitudinal direction in srs3 is shorter than that in the wild type. The number of cells of seeds in the longitudinal direction in srs3 was not very different from that in the wild type. The result suggests that the small and round seed phenotype of srs3 is due to a reduction in cell length of seeds in the longitudinal direction. The SRS3 protein, which is found in the crude microsomal fraction, is highly expressed in developing organs.
		+
		+	Rice yield potential is determined by several factors including seed size (or weight), number of panicles per plant and number of seeds per panicle (Song and Ashikari 2008, Takeda and Matsuoka 2008). Significant progress has been made in our understanding of regulation of seed formation through molecular and genetic studies, and this knowledge can potentially be used for the improvement of rice yield.
		+
		+	Causal genes of a large seed phenotype have been identified by quantitative trait locus analysis, namely GW2 encoding a RING-type protein which functions as an E3 ubiquitin ligase (Song et al. 2007), qSW5 encoding a novel protein with no known domain (Shoumura et al. 2008) and GS3 encoding a membrane protein with various conserved domains (Fan et al. 2006, Takano-Kai et al. 2009). Loss of GW2 and qSW5 function leads to enhanced seed width, and loss of GS3 function leads to enhanced seed length, both resulting in increased yield. Therefore, genes regulating seed size can potentially be used to increase overall yield. It will be important to reveal the biochemical pathways in which these genes function.
		+
		+	Causal genes of the small (or short) seed phenotype have also been identified as a group of seed size-regulating genes by map-based cloning, namely RGA1 (also named D1) encoding the heterotrimeric G protein α subunit (Ashikari et al. 1999, Fujisawa et al. 1999), D11 encoding a cytochrome P450 involved in brassinosteroid (BR) biosynthesis (Tanabe et al. 2005), D2 and BRD2 encoding an another type of cytochrome P450 involved in BR synthesis (Hong et al. 2003, Hong et al. 2005) and D61 (also named OsBRI1) encoding the BR receptor (Yamamuro et al. 2000). These results suggested that the G protein and BR signaling pathways were important in the regulation of seed size. After these studies, it was tested whether these genes were useful to improve the seed size in rice. When a genetically modified chimeric gene for a constitutively active form of the heterotrimeric G protein α subunit (QL) was introduced into the rice mutant d1, which is defective for the α subunit gene, the seed length and weight were substantially increased in the transformants (Oki et al. 2005). The result suggested that the enhancement of G protein signaling increased the seed size in rice. It was shown in another study that when a chimeric gene for a sterol C-22 hydroxylase in maize BR biosynthesis (Zm-CYP) was expressed in rice plants the seeds were heavier in the transformants (Wu et al. 2008). The result suggested that a gene controlling the BR level may be useful for increasing grain yield in crop plants. Thus, the utilization of seed size-regulating genes by genetic engineering approaches has opened up the way to produce improved rice plants with heavier seeds.
		+
		+	Although the heterotrimeric G protein and BR signaling pathways regulate seed size in rice, it is not clear whether other signaling pathway genes have similar effects. A search for new genes that regulate seed size would contribute to resolving this issue. It is likely that any newly discovered genes functioning in this manner would operate in the heterotrimeric G protein and BR signaling pathways. If this were the case, the new discoveries would help in analyzing the precise mechanism of these signaling pathways. If seed sizes could be increased by manipulating newly discovered genes, utilization of the new genes would also open up future possibilities for breeding improved rice plants with larger seeds. The presence of many unidentified genes regulating seed size has been shown in rice (Nagato and Yoshimura 1998). Previously we have reported the rough map position of a new causal gene for the small and round seed phenotype, one of the genes regulating seed size, namely SRS3 on chromosome 5 (Tanabe et al. 2007). Here we report that the SRS3 gene encodes a novel kinesin 13 protein.

	==Labs working on this gene==		==Labs working on this gene==

@@ Line 61: / Line 61: @@
    Mapping of Small and Round Seed 3 gene in rice
    Rice Genetics Newsletters, 2007, 23(): 56-58
 ==Structured Information==

@@ Line 4: / Line 4: @@
 ===Function===
 The causal gene of a novel small and round seed mutant phenotype (srs3) in rice was identified by map-based cloning and named the SRS3 gene. The SRS3 gene was grouped as a member of the kinesin 13 subfamily. The SRS3 gene codes for a protein of 819 amino acids that contains a kinesin motor domain and a coiled-coil structure. Using scanning electron microscopy, we determined that the cell length of seeds in the longitudinal direction in srs3 is shorter than that in the wild type. The number of cells of seeds in the longitudinal direction in srs3 was not very different from that in the wild type. The result suggests that the small and round seed phenotype of srs3 is due to a reduction in cell length of seeds in the longitudinal direction. The SRS3 protein, which is found in the crude microsomal fraction, is highly expressed in developing organs.
 ===Expression===

@@ Line 38: / Line 38: @@
 ==References==
-Please input cited references here.
+ Kanako Kitagawa;Shigeru Kurinami;Katsuyuki Oki;Yuki Abe;Tsuyu Ando;Izumi Kono;Masahiro Yano;Hidemi Kitano;Yukimoto Iwasaki
 ==Structured Information==