Flat sepals

Abstract

The cause of asymmetrical organ growth is differential distribution of a biochemical signal, such as a small RNA, protein or hormone. A recent study led by Hong Lilan from Zhejiang University uses the Arabidopsis sepal as a small and robust model of morphogenesis to understand what keeps it mostly flat during late flower development. The researchers isolated mutants with curved sepals bending outwards. The causal gene is VIP4, which encodes a component of the transcriptional regulator PAF1C. Its mutation causes an imbalance in growth rates and mechanical properties between abaxial and adaxial sides. A transcriptome analysis points to ARF3 and ARF4, two genes that are involved in auxin signalling and upregulated in the mutant, as potential downstream candidates, and a genetic approach confirmed this.

More experiments, including direct visualization of an ARF3–GFP (green fluorescent protein) construct, showed that transient and asymmetric distribution of ARF3, controlled directly by VIP4 (and indirectly via small mobile RNAs), is necessary for the sepal to stay flat. ARF3, in turn, affects auxin transport and signalling and cell wall stiffness through the expression of pectin methylesterases such as VGD1. So, quite counter-intuitively, in the wild-type sepal asymmetric ARF3 expression is needed for both sides to reach equivalent growth and stiffness. From an initial imbalance comes the symmetry that allows the sepal to grow flat.