Forward genetic screening for the improved production of fermentable sugars from plant biomass.

With their unique metabolism and the potential to produce large amounts of biomass, plants are an excellent bio-energy feedstock for a variety of industrial purposes. Here we developed a high-throughput strategy, using the model plant Arabidopsis thaliana, to identify mutants with improved sugar release from plant biomass. Molecular analysis indicates a variety of processes including starch degradation, cell wall composition and polar transport of the plant hormone auxin can contribute to this improved saccharification.

AMP1 and MP antagonistically regulate embryo and meristem development in Arabidopsis.

AUXIN RESPONSE FACTOR (ARF)-mediated signaling conveys positional information during embryonic and postembryonic organogenesis and mutations in MONOPTEROS (MP/ARF5) result in severe patterning defects during embryonic and postembryonic development. Here we show that MP patterning activity is largely dispensable when the presumptive carboxypeptidase ALTERED MERISTEM PROGRAM 1 (AMP1) is not functional, indicating that MP is primarily necessary to counteract AMP1 activity. Closer inspection of the single and double mutant phenotypes reveals antagonistic influences of both genes on meristematic activities throughout the Arabidopsis life cycle.

Overlapping and non-redundant functions of the Arabidopsis auxin response factors MONOPTEROS and NONPHOTOTROPIC HYPOCOTYL 4.

Transcription factors of the auxin response factor (ARF) family have been implicated in auxin-dependent gene regulation, but little is known about the functions of individual ARFs in plants. Here, interaction assays, expression studies and combinations of multiple loss- and gain-of-function mutants were used to assess the roles of two ARFs, NONPHOTOTROPIC HYPOCOTYL 4 (NPH4/ARF7) and MONOPTEROS (MP/ARF5), in Arabidopsis development. Both MP and NPH4 interact strongly and selectively with themselves and with each other, and are expressed in vastly overlapping domains.