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Galli, M.

Publications and source records attributed to Galli, M..

2 recordsLinked to original sources

The FUSED LEAVES1/ADHERENT1 Regulatory Module Is Required For Maize Cuticle Development And Organ Separation

In land plants all aerial epidermal cells are covered by the cuticle, an extracellular hydrophobic layer. The cuticle represents a primary barrier between cells and the external environment, provides protection against abiotic and biotic stresses, and prevents organ fusion during development. Here we report the cloning and characterization of a classic mutant of maize called adherent1 (ad1), first described a century ago, and we show that AD1 encodes a 3-KETOACYL-CoA SYNTHASE involved in the deposition of cuticular wax on the epidermis of leaves and inflorescences. ad1 mutants show decreased amounts of various wax components as well as a range of organ fusion defects during vegetative and reproductive development. Accordingly, we find that AD1 is strongly expressed in the epidermis of various developing organs where it is directly regulated by the MYB transcription factor FUSED LEAVES1 (FDL1), which in turn controls a series of additional genes involved in cuticle formation. Altogether, our results identify a major pathway of cuticle biosynthesis essential for the development of maize plants, and a key regulatory module that is conserved across monocot and eudicot species. One sentence summaryThe classic maize mutant adherent1, first isolated a century ago, is affected in an enzyme responsible for cuticle formation that is regulated by the MYB transcription factor FUSED LEAVES1.

plant biology

Telomere damage induces internal loops that generate telomeric circles

Extrachromosomal telomeric circles are commonly invoked as important players in telomere maintenance, but their origin has remained elusive. Using electron microscopy analysis on purified telomeres we show that, apart from known structures, telomeric repeats accumulate internal loops (i-loops), that occur in proximity of nicks and single-stranded DNA gaps. I-loops are induced by single-stranded damage at normal telomeres and represent the majority of telomeric structures detected in ALT (Alternative Lengthening of Telomeres) tumor cells. Our data indicate that i-loops form as a consequence of the exposure of single-stranded DNA at telomeric repeats. Finally, we show that these damage-induced i-loops can be excised to generate extrachromosomal telomeric circles resulting in loss of telomeric repeats. Our results identify damage-induced i-loops as a new intermediate in telomere metabolism and reveal a simple mechanism that links telomere damage with the accumulation of extrachromosomal telomeric circles and telomere erosion.

molecular biology