Abstract
Leaves of Arabidopsis develop from a shoot apical meristem grow along three (proximal–distal, adaxial–abaxial, and medial–lateral) axes and form a flat symmetric architecture. ASYMMETRIC LEAVES2 (AS2), a key regulator for leaf adaxial–abaxial partitioning, encodes a plant-specific nuclear protein and directly represses the abaxial-determining gene ETTIN/AUXIN RESPONSE FACTOR3 (ETT/ARF3). How AS2 could act as a critical regulator, however, has yet to be demonstrated, although it might play an epigenetic role. Here, we summarize the current understandings of the genetic, molecular, and cellular functions of AS2. A characteristic genetic feature of AS2 is the presence of a number of (about 60) modifier genes, mutations of which enhance the leaf abnormalities of as2. Although genes for proteins that are involved in diverse cellular processes are known as modifiers, it has recently become clear that many modifier proteins, such as NUCLEOLIN1 (NUC1) and RNA HELICASE10 (RH10), are localized in the nucleolus. Some modifiers including ribosomal proteins are also members of the small subunit processome (SSUP). In addition, AS2 forms perinucleolar bodies partially colocalizing with chromocenters that include the condensed inactive 45S ribosomal RNA genes. AS2 participates in maintaining CpG methylation in specific exons of ETT/ARF3. NUC1 and RH10 genes are also involved in maintaining the CpG methylation levels and repressing ETT/ARF3 transcript levels. AS2 and nucleolus-localizing modifiers might cooperatively repress ETT/ARF3 to develop symmetric flat leaves. These results raise the possibility of a nucleolus-related epigenetic repression system operating for developmental genes unique to plants and predict that AS2 could be a molecule with novel functions that cannot be explained by the conventional concept of transcription factors.
Highlights
Leaves develop from a shoot apical meristem (SAM) as lateral organs along three axes: proximal–distal, adaxial–abaxial, and medial–lateral [1,2,3,4,5,6,7]
The ASYMMETRIC LEAVES2 (AS2) and ASYMMETRIC LEAVES1 (AS1), which encode a protein with the plant-specific AS2/LOB domain and a protein with the MYB (SANT) domain, respectively, were originally identified as factors involved in symmetric leaf lamina formation [10,11,12,13]
The ectopic expression of class 1 Knotted1-like homeobox (KNOX) genes in as1 and as2 mutant plants results in reductions in the growth of leaf blades and petioles in Arabidopsis, and these phenotypes are suppressed by mutations of the class 1 KNOX genes, brevipedicellus, knat2, and knat6
Summary
Leaves develop from a shoot apical meristem (SAM) as lateral organs along three axes: proximal–distal, adaxial–abaxial, and medial–lateral [1,2,3,4,5,6,7]. The ectopic expression of class 1 Knotted1-like homeobox (KNOX) genes in as and as mutant plants results in reductions in the growth of leaf blades and petioles in Arabidopsis, and these phenotypes are suppressed by mutations of the class 1 KNOX genes, brevipedicellus (bp), knat, and knat6 These results indicate that the AS1 and AS2 genes of Arabidopsis are involved in the establishment of the proximal–distal axis through the repression of the class 1. ETTIN/AUXIN RESPONSE FACTOR3 (ETT/ARF3) and ARF4 specify both abaxial cell fate and the lateral growth of leaf lamina [31] Transcripts of both ETT/ARF3 and ARF4 are degraded by the small RNA tasiR-ARF, which is generated through a miR390 pathway in the presumptive adaxial domain and contributes to the determination of the adaxial cell fate [23]. Because a loss of adaxial–abaxial polarity is often accompanied by a defect of leaf lamina expansion, it is suggested that the lateral growth of the lamina could be related to the determination of adaxial–abaxial identity, as previously proposed [2,32]
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