Academic journal article Genetics

DICER-LIKE 1 and DICER-LIKE 3 Redundantly Act to Promote Flowering Via Repression of FLOWERING LOCUS C in Arabidopsis Thaliana

Academic journal article Genetics

DICER-LIKE 1 and DICER-LIKE 3 Redundantly Act to Promote Flowering Via Repression of FLOWERING LOCUS C in Arabidopsis Thaliana

Article excerpt

ABSTRACT

In Arabidopsis thaliana, DICER-LIKE 1 and DICER-LIKE 3 are involved in the generation of small RNAs. Double mutants between dicer-like 1 and dicer-like 3 exhibit a delay in flowering that is caused by increased expression of the floral repressor FLOWERING LOCUS C. This delayed-flowering phenotype is similar to that of autonomous-pathway mutants, and the flowering delay can be overcome by vernalization.

THE transition from vegetative to reproductive development is a highly regulated event in the plant life cycle. In Arabidopsis there are several pathways that influence time to flowering including the photoperiod, vernalization, autonomous, and FRIGIDA pathways. The photoperiod and vernalization pathways promote flowering in response to day length and the prolonged cold of winter, respectively. The vernalization pathway functions to epigenetically silence the strong floral repressor FLOWERING LOCUS C (FLC) (Bastow et al. 2004; Sung and Amasino 2004). The autonomous pathway acts to constitutively promote flowering by repressing FLC expression (for review see Simpson 2004), whereas FRIGIDA delays the floral transition by creating a vernalization requirement via upregulating FLC expression (Michaels and Amasino 1999; Sheldon et al. 1999). Because precise regulation of FLC is essential for proper timing of the floral transition, it is not surprising that FLC expression is controlled by multiple pathways.

Forward genetic screens have unveiled a large number of genes required for the floral transition (Sung and Amasino 2005). Components of the photoperiod pathway have been identified as mutants that flower at the same developmental stage regardless of the day length. Genes required for vernalization have been identified in screens for mutants that fail to flower rapidly after an extended exposure to cold temperatures. FRIGIDA pathway genes have been identified in screens for early- flowering mutants that block the ability of FRIGIDA to promote FLC expression. Finally, genes in the autonomous pathway have been identified as mutants that flower later than wild type in both inductive and noninductive photoperiods.

In higher plants, it is common for members of gene families to be functionally redundant. For such gene families, forward genetic screens are less likely to reveal the role of a single gene in a particular developmental process. Recently, Gasciolli et al. (2005) used a reverse genetics approach to determine possible functional redundancy among the four member DICER-LIKE (DCL) gene family. DCLs are ribonucleases that generate small RNA species from double-stranded RNA (Bernstein et al. 2001; Hutvagner et al. 2001). Each of the DCL enzymes generates predominantly a particular class of small RNA species. DCL1 is required for microRNA (miRNA) biogenesis (Park et al. 2002; Reinhart et al. 2002; Kurihara andWatanabe 2004), DCL2 generates viral small interfering RNAs (siRNA) (Xie et al. 2004), DCL3 forms heterochromatic siRNAs (Xie et al. 2004), and DCL4 is required for transactivating siRNA (ta-siRNA) biogenesis (Dunoyer et al. 2005; Gasciolli et al. 2005; Xie et al. 2005; Yoshikawaet al. 2005). Although DCL1- 4 have predominant roles in generating specific small RNA species, these DCLs can also have compensating functions (Gasciolli et al. 2005; Blevins et al. 2006; Deleris et al. 2006). For example, TAS1-3 mRNA levels in dcl4 mutants are lower than those in Columbia (Col), whereas levels in dcl2 or dcl3 are indistinguishable from those in wild type. However, double mutants between dcl4 and either dcl2 or dcl3 result in a further loss of TAS1-3 mRNAexpression, indicating that in the absence of DCL4, DCL2 and DCL3 process siRNAs that are otherwise primarily processed by DCL4 (Gasciolli et al. 2005). Thus, double and triple dcl mutant combinations, created in the Col accession, result in phenotypes not observed in the single mutants (Gasciolli et al. 2005). For example, a double mutant between a weak dcl1 allele (dcl1 null alleles are lethal; Schauer et al. …

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