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Gene Review:

CLV2 - leucine-rich repeat receptor-like protein...

Arabidopsis thaliana

Synonyms: AtRLP10, Receptor Like Protein 10, T8F5.16, T8F5_16, clavata 2

Jeong, S. et al., Shepard, K.A. et al., Kayes, J.M. et al., Hobe, M. et al., Rojo, E. et al., et al.

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High impact information on CLV2

Crossing of the CLE19 overexpression line with clv mutants confirms the involvement of CLV2 [1].
Other components of the CLV1 signaling pathway include the secreted putative ligand CLV3 and the receptor-like protein CLV2 [2].
We used genetic and immunological assays to show that CLV3 localizes to the apoplast and that export to the extracellular space is required for its function in activating the CLV1/CLV2 receptor complex [3].
We isolated the CLV2 gene and found that it encodes a receptor-like protein (RLP), with a presumed extracellular domain composed of leucine-rich repeats similar to those found in plant and animal receptors, but with a very short predicted cytoplasmic tail [4].
In addition, the chromosomal region in which CLV2 is located contains an extremely high rate of polymorphism, with 50 nucleotide and 15 amino acid differences between Landsberg erecta and Columbia ecotypes within the CLV2 coding sequence [4].

Biological context of CLV2

These alterations include flower-to-shoot transformations, as well as a nearly complete suppression of the flower phenotypes, indicating that the requirement for CLV2 changes in response to different physiological conditions [5].
Most alleles at CLV2 are found in one of three haplotype groups of moderate (>15%) frequency [6].
The levels and patterns of nucleotide variation were assessed for CLV2 and 10 flanking genes that together span a 40-kb region of chromosome I. A total of 296 out of 7959 sequenced nucleotide sites were polymorphic [6].
CLV2 has the highest levels of nucleotide variation in this region, a significant excess of intermediate frequency polymorphisms, and significant levels of intragenic linkage disequilibrium [6].

Anatomical context of CLV2

In Arabidopsis, stem cells in shoot and floral meristems secrete CLAVATA3, a member of the CLE protein family that activates the CLV1/CLV2 receptor complex in underlying cells to restrict the size of the stem cell population [7].

Other interactions of CLV2

We present genetic analysis that CLV2 may function in the same pathway as CLV1 and CLV3 in the regulation of meristem development, but function separately in the regulation of organ development [5].

Analytical, diagnostic and therapeutic context of CLV2

Sequence analysis suggests that the charged residue in the predicted transmembrane domain of CLV2 may be a common feature of plant RLPs and RLKs [4].

References

The 14-amino acid CLV3, CLE19, and CLE40 peptides trigger consumption of the root meristem in Arabidopsis through a CLAVATA2-dependent pathway. Fiers, M., Golemiec, E., Xu, J., van der Geest, L., Heidstra, R., Stiekema, W., Liu, C.M. Plant Cell (2005) [Pubmed]
CLAVATA1 dominant-negative alleles reveal functional overlap between multiple receptor kinases that regulate meristem and organ development. Diévart, A., Dalal, M., Tax, F.E., Lacey, A.D., Huttly, A., Li, J., Clark, S.E. Plant Cell (2003) [Pubmed]
CLV3 is localized to the extracellular space, where it activates the Arabidopsis CLAVATA stem cell signaling pathway. Rojo, E., Sharma, V.K., Kovaleva, V., Raikhel, N.V., Fletcher, J.C. Plant Cell (2002) [Pubmed]
The Arabidopsis CLAVATA2 gene encodes a receptor-like protein required for the stability of the CLAVATA1 receptor-like kinase. Jeong, S., Trotochaud, A.E., Clark, S.E. Plant Cell (1999) [Pubmed]
CLAVATA2, a regulator of meristem and organ development in Arabidopsis. Kayes, J.M., Clark, S.E. Development (1998) [Pubmed]
Molecular population genetics of the Arabidopsis CLAVATA2 region. The genomic scale of variation and selection in a selfing species. Shepard, K.A., Purugganan, M.D. Genetics (2003) [Pubmed]
Loss of CLE40, a protein functionally equivalent to the stem cell restricting signal CLV3, enhances root waving in Arabidopsis. Hobe, M., Müller, R., Grünewald, M., Brand, U., Simon, R. Dev. Genes Evol. (2003) [Pubmed]

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