Difference between revisions of "Os06g0724900"
| Line 5: | Line 5: | ||
ILA1 is a functional kinase with Ser/Thr kinase activity.ILA1 is a key factor regulating mechanical tissue formation at the leaf lamina joint and is involved in mechanical tissue formation in the leaf lamina joint.<ref name="ref1" / > | ILA1 is a functional kinase with Ser/Thr kinase activity.ILA1 is a key factor regulating mechanical tissue formation at the leaf lamina joint and is involved in mechanical tissue formation in the leaf lamina joint.<ref name="ref1" / > | ||
===Expression=== | ===Expression=== | ||
| − | ILA1 is predominantly resident in the nucleus and expressed in the vascular bundles of leaf lamina joints.The leaf angle of WT is increased compared that of ila1. But the increased leaf angle of ila1 is not due to altered BR. ILA1 mutation significantly represses the expression of genes involved in cell wall synthesis and consequently causes the increased leaf responses. <ref name="ref2"/>ILA1 encodes a putative MAPKKK protein with a length of 564 amino acids and a molecular mass of 63 kD. According to the Pfam database, the deduced ILA1 has an N-terminal ACT domain (PF01842) and a C-terminal kinase domain (PF07714), which likely confer a protein regulatory feature and kinase activity, respectively. Sequence alignment of ILA1 with several identified MAPKKKs from three representative plant species | + | ILA1 is predominantly resident in the nucleus and expressed in the vascular bundles of leaf lamina joints.ILA1Encodes a Group C Raf-Like MAPKKK with Ser/Thr Kinase Activity.Thermal asymmetric interlaced PCR showed that the increased leaf angle ofila1arises from a T-DNA insertion in Os06g50920.Because nuclear localization is a significant feature of transcription factors, GFP is fused to the N terminus of IIP2 and IIP4 and transformed the rice protoplasts. Detection of thefusion proteins in the nuclei of the transformed cells suggest that IIP2 and IIP4 are nuclear-localized proteins. To confirm the sequence identity ofILA1, a complementation test is performed by transforming theila1 mutant with an 8.8-kbgenomic region that included the complete open reading frame(ORF) and putative promoter region for ILA1 (pILA1). All of the complementation lines show the wild-type leaf inclination,suggesting that Os06g50920 is ILA1.The leaf angle of WT is increased compared that of ila1. But the increased leaf angle of ila1 is not due to altered BR. ILA1 mutation significantly represses the expression of genes involved in cell wall synthesis and consequently causes the increased leaf responses. <ref name="ref2"/>ILA1 encodes a putative MAPKKK protein with a length of 564 amino acids and a molecular mass of 63 kD. According to the Pfam database, the deduced ILA1 has an N-terminal ACT domain (PF01842) and a C-terminal kinase domain (PF07714), which likely confer a protein regulatory feature and kinase activity, respectively. Sequence alignment of ILA1 with several identified MAPKKKs from three representative plant species reveal that the characteristic features for MAPKKK proteins, including all of the 11 subdomains and a Lys in the ATP binding site, are highly conserved in ILA1. ILA1 represents a potentially unique paradigm in the regulation of leaf angle in rice. QRT-PCR analysis reveal high expression levels of ILA1 in both leaves and leaf lamina joints. However,ila1 exhibits a visible phenotype mainly in its leaf lamina joints butnot in its leaves. To confirm the interaction of ILA1 with IIPs, the ILA1 protein is split into kinase (ILA1K) and regulatory (ILA1R) domains andsubjected to interaction analysis.The kinase domain of ILA1 is involved in the interaction with IIPs in subfamily B, but not with IIPs in subfamily A.And the N-terminal regulatory domain interacts with IIPs. |
| + | IIPs,the Likely Targets of ILA1, are Nuclear Proteins with Transactivation Activity.In light of the evidence for interaction between ILA1 and IIPs, it seemed that IIPs may be the phosphorylated substrates of ILA1.IIP4 is selected as a representative to test this hypothesis.IIP4 fused to a polyhistidine tag (His-IIP4)is purified and incubated | ||
| + | with GST-ILA1 for an in vitro kinase activity assay. Radioactively labeled IIP4 is detected. These results reveal that IIP4 is a phosphorylated substrate of ILA1, as is likely the case for the other IIPs.The Gene Ontology database annotate IIPs as putative transcription factors. | ||
| + | |||
| + | ===Evolution=== | ||
| − | |||
| − | |||
You can also add sub-section(s) at will. | You can also add sub-section(s) at will. | ||
possible mechanism of ILA1 action | possible mechanism of ILA1 action | ||
Identification of ILA1 phosphorylation substrates is critical for understanding the signal transduction pathway of a Group C Raflike MAPKKK member. Through yeast two-hybrid screening of the cDNA library, six interaction proteins (IIPs) were found; these IIPs consist of a small family with unknown functions. The interactions were further confirmed by the BiFC and Co-IP analyses of a representative IIP. More importantly,ILA1 could phosphorylate an IIP in vitro. IIPs are thus likely to be the authentic downstream targets of ILA1. IIPs may act as transcription factors for they were regarded as putative transcription factors by bioinformatic analysis;they are nuclear localized in rice and they showed transactivation activity in yeast. | Identification of ILA1 phosphorylation substrates is critical for understanding the signal transduction pathway of a Group C Raflike MAPKKK member. Through yeast two-hybrid screening of the cDNA library, six interaction proteins (IIPs) were found; these IIPs consist of a small family with unknown functions. The interactions were further confirmed by the BiFC and Co-IP analyses of a representative IIP. More importantly,ILA1 could phosphorylate an IIP in vitro. IIPs are thus likely to be the authentic downstream targets of ILA1. IIPs may act as transcription factors for they were regarded as putative transcription factors by bioinformatic analysis;they are nuclear localized in rice and they showed transactivation activity in yeast. | ||
| + | |||
==Labs working on this gene== | ==Labs working on this gene== | ||
# National Key Laboratory of Crop Genetic Improvement and National Center for Plant Gene Research (Wuhan), Huazhong | # National Key Laboratory of Crop Genetic Improvement and National Center for Plant Gene Research (Wuhan), Huazhong | ||
| Line 21: | Line 24: | ||
# Department of Biochemistry and Molecular Biology, University of Georgia, Athens, Georgia | # Department of Biochemistry and Molecular Biology, University of Georgia, Athens, Georgia | ||
| − | == | + | ==references== |
1.Jing Ning;Baocai Zhang;Nili Wang;Yihua Zhou;Lizhong Xiong.Increased Leaf Angle1, a Raf-Like MAPKKK That Interacts with a Nuclear Protein Family, Regulates Mechanical Tissue Formation in the Lamina Joint of Rice.The Plant Cell, 2011, 23(12): 4334-4347 | 1.Jing Ning;Baocai Zhang;Nili Wang;Yihua Zhou;Lizhong Xiong.Increased Leaf Angle1, a Raf-Like MAPKKK That Interacts with a Nuclear Protein Family, Regulates Mechanical Tissue Formation in the Lamina Joint of Rice.The Plant Cell, 2011, 23(12): 4334-4347 | ||
2.Wang, L., Xie, W., Chen, Y., Tang, W., Yang, J., Ye, R., Liu, L., Lin, Y.,Xu, C., Xiao, J., and Zhang, Q.(2010). A dynamic gene expression atlas covering the entire life cycle of rice. Plant J.61:752–766. | 2.Wang, L., Xie, W., Chen, Y., Tang, W., Yang, J., Ye, R., Liu, L., Lin, Y.,Xu, C., Xiao, J., and Zhang, Q.(2010). A dynamic gene expression atlas covering the entire life cycle of rice. Plant J.61:752–766. | ||
| + | |||
==Structured Information== | ==Structured Information== | ||
{{JaponicaGene| | {{JaponicaGene| | ||
Revision as of 02:38, 8 June 2014
Please input one-sentence summary here.
Contents
Annotated Information
Function
ILA1 is a functional kinase with Ser/Thr kinase activity.ILA1 is a key factor regulating mechanical tissue formation at the leaf lamina joint and is involved in mechanical tissue formation in the leaf lamina joint.<ref name="ref1" / >
Expression
ILA1 is predominantly resident in the nucleus and expressed in the vascular bundles of leaf lamina joints.ILA1Encodes a Group C Raf-Like MAPKKK with Ser/Thr Kinase Activity.Thermal asymmetric interlaced PCR showed that the increased leaf angle ofila1arises from a T-DNA insertion in Os06g50920.Because nuclear localization is a significant feature of transcription factors, GFP is fused to the N terminus of IIP2 and IIP4 and transformed the rice protoplasts. Detection of thefusion proteins in the nuclei of the transformed cells suggest that IIP2 and IIP4 are nuclear-localized proteins. To confirm the sequence identity ofILA1, a complementation test is performed by transforming theila1 mutant with an 8.8-kbgenomic region that included the complete open reading frame(ORF) and putative promoter region for ILA1 (pILA1). All of the complementation lines show the wild-type leaf inclination,suggesting that Os06g50920 is ILA1.The leaf angle of WT is increased compared that of ila1. But the increased leaf angle of ila1 is not due to altered BR. ILA1 mutation significantly represses the expression of genes involved in cell wall synthesis and consequently causes the increased leaf responses. [1]ILA1 encodes a putative MAPKKK protein with a length of 564 amino acids and a molecular mass of 63 kD. According to the Pfam database, the deduced ILA1 has an N-terminal ACT domain (PF01842) and a C-terminal kinase domain (PF07714), which likely confer a protein regulatory feature and kinase activity, respectively. Sequence alignment of ILA1 with several identified MAPKKKs from three representative plant species reveal that the characteristic features for MAPKKK proteins, including all of the 11 subdomains and a Lys in the ATP binding site, are highly conserved in ILA1. ILA1 represents a potentially unique paradigm in the regulation of leaf angle in rice. QRT-PCR analysis reveal high expression levels of ILA1 in both leaves and leaf lamina joints. However,ila1 exhibits a visible phenotype mainly in its leaf lamina joints butnot in its leaves. To confirm the interaction of ILA1 with IIPs, the ILA1 protein is split into kinase (ILA1K) and regulatory (ILA1R) domains andsubjected to interaction analysis.The kinase domain of ILA1 is involved in the interaction with IIPs in subfamily B, but not with IIPs in subfamily A.And the N-terminal regulatory domain interacts with IIPs.
IIPs,the Likely Targets of ILA1, are Nuclear Proteins with Transactivation Activity.In light of the evidence for interaction between ILA1 and IIPs, it seemed that IIPs may be the phosphorylated substrates of ILA1.IIP4 is selected as a representative to test this hypothesis.IIP4 fused to a polyhistidine tag (His-IIP4)is purified and incubated
with GST-ILA1 for an in vitro kinase activity assay. Radioactively labeled IIP4 is detected. These results reveal that IIP4 is a phosphorylated substrate of ILA1, as is likely the case for the other IIPs.The Gene Ontology database annotate IIPs as putative transcription factors.
Evolution
You can also add sub-section(s) at will. possible mechanism of ILA1 action Identification of ILA1 phosphorylation substrates is critical for understanding the signal transduction pathway of a Group C Raflike MAPKKK member. Through yeast two-hybrid screening of the cDNA library, six interaction proteins (IIPs) were found; these IIPs consist of a small family with unknown functions. The interactions were further confirmed by the BiFC and Co-IP analyses of a representative IIP. More importantly,ILA1 could phosphorylate an IIP in vitro. IIPs are thus likely to be the authentic downstream targets of ILA1. IIPs may act as transcription factors for they were regarded as putative transcription factors by bioinformatic analysis;they are nuclear localized in rice and they showed transactivation activity in yeast.
Labs working on this gene
- National Key Laboratory of Crop Genetic Improvement and National Center for Plant Gene Research (Wuhan), Huazhong
Agricultural University, Wuhan , China
- State Key Laboratory of Plant Genomics and National Centre for Plant Gene Research (Beijing), Institute of Genetics and Developmental Biology, Chinese Academy of Sciences, Beijing , China
- Complex Carbohydrate Research Center, University of Georgia, Athens, Georgia
- Department of Plant Biology, University of Georgia, Athens, Georgia
- Department of Biochemistry and Molecular Biology, University of Georgia, Athens, Georgia
references
1.Jing Ning;Baocai Zhang;Nili Wang;Yihua Zhou;Lizhong Xiong.Increased Leaf Angle1, a Raf-Like MAPKKK That Interacts with a Nuclear Protein Family, Regulates Mechanical Tissue Formation in the Lamina Joint of Rice.The Plant Cell, 2011, 23(12): 4334-4347 2.Wang, L., Xie, W., Chen, Y., Tang, W., Yang, J., Ye, R., Liu, L., Lin, Y.,Xu, C., Xiao, J., and Zhang, Q.(2010). A dynamic gene expression atlas covering the entire life cycle of rice. Plant J.61:752–766.
Structured Information
| Gene Name |
Os06g0724900 |
|---|---|
| Description |
Amino acid-binding ACT domain containing protein |
| Version |
NM_001065152.1 GI:115470035 GeneID:4342105 |
| Length |
5914 bp |
| Definition |
Oryza sativa Japonica Group Os06g0724900, complete gene. |
| Source |
Oryza sativa Japonica Group ORGANISM Oryza sativa Japonica Group
Eukaryota; Viridiplantae; Streptophyta; Embryophyta; Tracheophyta;
Spermatophyta; Magnoliophyta; Liliopsida; Poales; Poaceae; BEP
clade; Ehrhartoideae; Oryzeae; Oryza.
|
| Chromosome | |
| Location |
Chromosome 6:31694442..31700355 |
| Sequence Coding Region |
31694488..31694678,31695034..31695148,31695248..31695333,31695455..31695565,31696057..31696111 |
| Expression | |
| Genome Context |
<gbrowseImage1> name=NC_008399:31694442..31700355 source=RiceChromosome06 preset=GeneLocation </gbrowseImage1> |
| Gene Structure |
<gbrowseImage2> name=NC_008399:31694442..31700355 source=RiceChromosome06 preset=GeneLocation </gbrowseImage2> |
| Coding Sequence |
<cdnaseq>atggaccacggcggtcaggtctctcccgtgccggcgacggcgacggcgccgcggaaggtcaggagagaacacatgaggctgggggtgtaccacgacgtgctgcagcggctcagggacgccggcgcgcccgaggccctcgcgccggacttcgccgagaagctctggacgcacttccaccgcttcaacgccagttatgccatggatgtcaatgttgagagggcagaagacgttctgatgcacatgaagctgcttgagaaggctatccatcctgaaaatcagcctgccttctcagtgagaattgttcaggttcctctagatattgatgcgagtgaagccgattcacagtcaaacatcactgaagatgacaactgtcctacgccaagaacaccagctgaacaccctgcacctatttttggctctaccacagcccttaaggctcttgttcgtcaagcaagcagcaagaacctcctggatgacaaccaagacatagatgctattctcagacccatgcatgagatcacctttgcatctgatgacaaaccaaagggccttactcaactgtcttcacttctaggcaatctcaatcttgatatcaaagaagtacatgcactttcaacaaatgatggttacttcttagatattttcatcgtaatcggatgggatcacaaggaaacccaacttctcgaagaagcgttggagaaggaaattcacaattacgaaccacagatgccctcaaaatcttcttgctggcctcctgaattagcaggcaagcagtctttgattaactcgcaagtcaaccatgttcagatacctaaagataacacagatgaatgggaaattaacttcgacgtattggatattcaagagaaagtggcatctggaacgtatggtgatctctatcgcggtacatattttggtgaagatgtcgcaattaaggtgctcaagtcagatcgtcttaatgagaacatgcaggaggaatttaacgaagaagtattcatcatgaggaagattcgtcataagaacattgttcgatttcttggggcatgcaccaaatccccaaccttatgtattgtcacagagtttatgaaaaatggaagtgtttacgactaccttcataagcgtaaaggttccttcaaacttcccagtctgcttaaagctgcagttgatatatcaaaagggatgaactatttacaccaaaataaaattattcatcgagacttgaagacagcaaaccttcttatggatgagcacgagcttatcaaggttgctgattttggtgttgcacgtgtaaaagctgaatcagggattatgactgccgaaactggtacatatcgttggatggctcctgaggttattgagcataagccatatgattcaaaggctgatgtctttagctttggtgttgttttgtgggagctacttacgggaaagattcctcacgagtttctaacaccactccaagcagccataggtgttgttcaagagggtttaagaccagttattcccaaggccacagatcctaaactcgcgctgttacttgagagttgctggcagcaaaatgctgtcaacagaccagactttgtacaaattttgcaaaagcttgatgaaattgctggggagcatggcattgatcttacccatccccataaagagaaggagaaaggaggcttctttacttttgggaaggtccattga</cdnaseq> |
| Protein Sequence |
<aaseq>MDHGGQVSPVPATATAPRKVRREHMRLGVYHDVLQRLRDAGAPE ALAPDFAEKLWTHFHRFNASYAMDVNVERAEDVLMHMKLLEKAIHPENQPAFSVRIVQ VPLDIDASEADSQSNITEDDNCPTPRTPAEHPAPIFGSTTALKALVRQASSKNLLDDN QDIDAILRPMHEITFASDDKPKGLTQLSSLLGNLNLDIKEVHALSTNDGYFLDIFIVI GWDHKETQLLEEALEKEIHNYEPQMPSKSSCWPPELAGKQSLINSQVNHVQIPKDNTD EWEINFDVLDIQEKVASGTYGDLYRGTYFGEDVAIKVLKSDRLNENMQEEFNEEVFIM RKIRHKNIVRFLGACTKSPTLCIVTEFMKNGSVYDYLHKRKGSFKLPSLLKAAVDISK GMNYLHQNKIIHRDLKTANLLMDEHELIKVADFGVARVKAESGIMTAETGTYRWMAPE VIEHKPYDSKADVFSFGVVLWELLTGKIPHEFLTPLQAAIGVVQEGLRPVIPKATDPK LALLLESCWQQNAVNRPDFVQILQKLDEIAGEHGIDLTHPHKEKEKGGFFTFGKVH</aaseq> |
| Gene Sequence |
<dnaseqindica>47..237#593..707#807..892#1014..1124#1616..1670#1789..1899#2809..2865#3309..3478#3565..3672#4105..4178#4283..4456#4648..4745#4964..5044#5136..5189#5396..5530#5624..5698#tgcagcgtttgcagtcgttgtgcgcatttcgtcgaacaggtcggcgatggaccacggcggtcaggtctctcccgtgccggcgacggcgacggcgccgcggaaggtcaggagagaacacatgaggctgggggtgtaccacgacgtgctgcagcggctcagggacgccggcgcgcccgaggccctcgcgccggacttcgccgagaagctctggacgcacttccaccgcttcaacgccaggttcttaatacaaccaccctgcgcatcattgctgccaaaaactcgtgtctgcatgtttgatttcgtctctaagattgatctttgatcgaatgcatacggggcactgttcaaactaaaatttaccctctgtgatgattttcaagtgtcaggcctgtgaatccgaatcagggcctgaaatggaagatgaatttggctaacatttctgagtctaagcacactaggagttggctagagtctaaatttcgatgctctactttttgatatgggggcgctcccagtgcctaatttgttcttttcgaattgctggttccaaatatgatcaactctattcttgttcttcgatttgatatggcagttatgccatggatgtcaatgttgagagggcagaagacgttctgatgcacatgaagctgcttgagaaggctatccatcctgaaaatcagcctgccttctcagtgagaattgttcaggtacatttacgccaaaaaggagaacagcttcgattggtttgctcatgttttgcagcagtatatctgtggtatgtttctgaagcaaacattgctgtgcaggttcctctagatattgatgcgagtgaagccgattcacagtcaaacatcactgaagatgacaactgtcctacgccaagaacaccagcgtatgtcctttaagattgctatgtatcatgacatgttgttatatttttctatttgtgcttagtgctagtatttatattctgttttttctccccttatatttctgtttgtttgatttctcagtgaacaccctgcacctatttttggctctaccacagcccttaaggctcttgttcgtcaagcaagcagcaagaacctcctggatgacaaccaagacatagatgctattctcaggtttgcatatttatagttactaggtcctgaaattttctcatttacctatgcacttttttctctttgcactttcggatttttctgttttagacattcatttttaattcaaatatcactaattagctcattttgctgttacttgatgttgtgtttattcctttttttcagtcagagtgtggttatttctttaaaacactaatcagtgagactatgatatttagaaccatttcttctgtttcattgctgtagttctatttaacatgcacatatgttgaagactgtttatgtcagtacatggtattcttctttcatttatcgtctttgtactctgagatttgggaataagtgagtgcaattccacaatctatgcttctctcttttcaaaaaaaaaaaaacattctatgcatctgaataaaaagctggggaggagcataacatgatgcttattcgtttctctcttttcccttggctgcaaatttcttatcttgcagacccatgcatgagatcacctttgcatctgatgacaaaccaaagggccttactcaagtaagttttcttactccaaacttctggaatagcaaaaccgaggattcattactatggaagaatttgttacacatgttttgagagccttcctgatactatcggttgcatattatttcagctgtcttcacttctaggcaatctcaatcttgatatcaaagaagtacatgcactttcaacaaatgatggttacttcttagatattttcatcgtaatcggatgggatcacaaggtattgtttggtccatttctctactcaggaaacatttgattaaaaattcttaaccatattctccctctatcccaaaatataagcactcaggtgcttttcacgaggatcaaggagagacatgaaattaaatgggggatatttgtcactggttgagatgtggaagtaagtagagaaacaaaataagagatggttgtgattggttgagatgagggaataggtggagaagtagctatattttaggacaaaatttgaatgctcaaagtagctctattttgggatggagggagtagttgtctgtcttgcttcctacatgtaaggacatctaagtattcatgatctcaacattcattcatacttttaccattgttttgcatgaattgctatgaatccaactgagtttatatatattctatgacctttgatctactaattttctagtaaaattttatagcacaatgtccataatataggattgtctaagaccatatcccaaaccagttttgaaccagtacatcttatctatgctttgtaatcccaaagcatttgcctaaatgccatttagagtttatttgcctgttcatgaagagctcaagaaaactctgagaaaaaaatgttatttgactactgttaatggttatcagtgaacttataggcacgtagttgcatattattggattgcacaggaatattagaaacagcaaaaaatgatttttgcatattttgggctgacaaaccggaaagctttattgttccctttttagctaccttaaacaattattttgtgaaaatcagccgaaaaattggtgggagttctgttactgtaattttaaattcgcaaggatctgttccctttgctgaataagaatatgcttgttagaaaggaggataattattcttttgattttacaggaaacccaacttctcgaagaagcgttggagaaggaaattcacaattacgaaccacaggtagagtttcattgatattcctctttattttctcactataattaaaatgcattagagctttgtttgctctgttgccagaaatgtttaaaaaaatatgcagaaactagataaaatatagtgctgaagtcaaccgaaaacaaaataaaagaagtttaagattttcctgcccaccatacgatagtactgcacaatcttaaaggtcagtagtttacatcacaagctcttgaaggcgcataagaaaagggggattcagaagtattggaatagtatgctttgttctagatcaagaagatatggttacatcatagaatatgatgttctcttgacaaataacaattcagttcgtttattaagctattgtatttctctctctgccaatactgattacagcatttctatatttcctaatacttactgttttcattgttgaaaattttctgcagatgccctcaaaatcttcttgctggcctcctgaattagcaggcaagcagtctttgattaactcgcaagtcaaccatgttcagatacctaaagataacacagatgaatgggaaattaacttcgacgtattggatattcaagagaaagtggcatctggaacgtatggtgatctgtgagtatcctgttgttgcgttgcatggaaccttcagtctgttagacattgcctcaagagtcattcttcctcccttgaggttgcagctatcgcggtacatattttggtgaagatgtcgcaattaaggtgctcaagtcagatcgtcttaatgagaacatgcaggaggaatttaacgaagaagtattcatcatgaggttagtaataaaataaagatatgggattctcaaaaccaaaaaaaataaaaaggaaaagtaaataaacctgtaatgtcgaatgcctagcaagctcatctagtaactaagccatcgctgtataaggtgtagcgagatgactttcccaatggcttcgagtcattcattgaaatgtacaagtcgtttatgaacacatcatgtgaatcatattatgcaaagttttgtctgaaccatagaaaaacttgcacaaacttaatcatagcatacagcacaatctaagaatttgacaacattacagctatacaaccttaagtaattcagcagtctatttggtaagctgattgaagttacatagacaattctttatcagagccttttccctggaaagtaacacatctctttgaccatgttgccgatggaactgccaaattctaggaagattcgtcataagaacattgttcgatttcttggggcatgcaccaaatccccaaccttatgtattgtcacaggtaaaatgaatacagatgccaattccttttaattatgcagattttgcccatttatatgtgatggtgttatccccttacattttggaatttacatatttcaccagagtttatgaaaaatggaagtgtttacgactaccttcataagcgtaaaggttccttcaaacttcccagtctgcttaaagctgcagttgatatatcaaaagggatgaactatttacaccaaaataaaattattcatcgagacttgaagacagcaaaccttcttatggatgagcacgaggcaagacttttgatcgctctgtagcttaatcctgagtagtcattaacgtaattactttataatgtggcttgatgatcagggataaacatagtttttcatggcctgtagtttgttggtattgctttctttgcagaactgttgttgtcacaattattttcatgattaaactgatatggatgaatctttttcagcttatcaaggttgctgattttggtgttgcacgtgtaaaagctgaatcagggattatgactgccgaaactggtacatatcgttggatggctcctgaggtaatctttttaaattatatattcaagtgaaatcccagttttgcatagaggacatagcaaatgtttcccttttcttctctaatgatgatagtttatccaatttaatggtaaattttccaaaccatcgcacaactttctcaaaagaaattggagagctaagcaacagattgggatacatgtttttcacatctcagatctatgcaacgctttttatgtaggttattgagcataagccatatgattcaaaggctgatgtctttagctttggtgttgttttgtgggagctacttacgggaaaggtattattgattcattggctagtgattttctcttggaaatataagtttttgctgccaacatacttatgttttttttaacatactttactagattcctcacgagtttctaacaccactccaagcagccataggtgttgttcaagaggtcaagagctaagctgaattttttttttcttgttactatttgacataacaaatgcagctccaatatcataatgtggacatcttttctttatgctttcctacttcataaaactacttatgttatagttcacattttttaaaagaggttatcttatggttcacatttcacaatctttcaatcaagtaaacaaacggttgacatggcagggtttaagaccagttattcccaaggccacagatcctaaactcgcgctgttacttgagagttgctggcagcaaaatgctgtcaacagaccagactttgtacaaattttgcaaaagcttgatgaaattgctggggaggtaggcatctgtgacctatttaccatttcatgaaatcccaaattttcatattcttgcttgatggcctgatgggtgtatgtaacgtactgacagcatggcattgatcttacccatccccataaagagaaggagaaaggaggcttctttacttttgggaaggtccattgatgaaattcttgtatcatatctaaagttgcacattgtttttctgcagctactttctcgatagatttctctgaaagatactgtgtattcaggggtttattattgtacagtgtggtagctgactggcagatcacttagccgccatttgtcttttccaccaaatgtaaagcaagtacccgtgtaattttcaattgctgtatagtgtatactacggaaagc</dnaseqindica> |
| External Link(s) |
- ↑ Cite error: Invalid
<ref>tag; no text was provided for refs namedref2
