Mutation of an Arabidopsis NatB N-alpha-terminal acetylation complex component causes pleiotropic developmental defects.

N-α-terminal acetylation is one of the most common, but least understood modifications of eukaryotic proteins. Although a high degree of conservation exists between the N-α-terminal acetylomes of plants and animals, very little information is available on this modification in plants. In yeast and humans, N-α-acetyltransferase complexes include a single catalytic subunit and one or two auxiliary subunits.

Arabidopsis TRANSCURVATA1 encodes NUP58, a component of the nucleopore central channel.

The selective trafficking of proteins and RNAs through the nuclear envelope regulates nuclear-cytoplasmic segregation of macromolecules and is mediated by nucleopore complexes (NPCs), which consist of about 400 nucleoporins (Nups) of about 30 types. Extensive studies of nucleoporin function in yeast and vertebrates showed that Nups function in nucleocytoplasmic trafficking and other processes. However, limited studies of plant Nups have identified only a few mutations, which cause pleiotropic phenotypes including reduced growth and early flowering.

The RON1/FRY1/SAL1 gene is required for leaf morphogenesis and venation patterning in Arabidopsis.

To identify genes involved in vascular patterning in Arabidopsis (Arabidopsis thaliana), we screened for abnormal venation patterns in a large collection of leaf shape mutants isolated in our laboratory. The rotunda1-1 (ron1-1) mutant, initially isolated because of its rounded leaves, exhibited an open venation pattern, which resulted from an increased number of free-ending veins. We positionally cloned the RON1 gene and found it to be identical to FRY1/SAL1, which encodes an enzyme with inositol polyphosphate 1-phosphatase and 3' (2'),5'-bisphosphate nucleotidase activities and has not, to our knowledge, previously been related to venation patterning.

Role of HEMIVENATA and the Ubiquitin Pathway in Venation Pattern Formation.

Elegant work by others has highlighted the importance of auxin transport in venation patterning, an idea substantiated by the severe effects of auxin polar transport inhibitors and by the mutant phenotype and expression patterns associated with the auxin efflux transporter PIN-FORMED1 (PIN1). It is striking, therefore, that little attention has been paid to the venation patterns of mutants insensitive to this hormone, since both auxin transport and perception are crucial components in theoretical models of vascular patterning. Our finding that HEMIVENATA (HVE) is the same gene as CAND1 confirms the role of ubiquitin-mediated auxin perception in vascular patterning and sets the stage for a re-examination of the leaf venation phenotypes of other auxin-resistant mutants and additional components of the ubiquitin pathway.

The HVE/CAND1 gene is required for the early patterning of leaf venation in Arabidopsis.

The hemivenata-1 (hve-1) recessive allele was isolated in a search for natural variations in the leaf venation pattern of Arabidopsis thaliana, where it was seen to cause extremely simple venation in vegetative leaves and cotyledons, increased shoot branching, and reduced root waving and fertility, traits that are reminiscent of some mutants deficient in auxin signaling. Reduced sensitivity to exogenous auxin was found in the hve-1 mutant, which otherwise displayed a wild-type response to auxin transport inhibitors. The HVE gene was positionally cloned and found to encode a CAND1 protein.