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Motivated by humans' ability to adapt skills in the learning of new ones, this paper presents AdaptNet, an approach for modifying the latent space of existing policies to allow new behaviors to be quickly learned from like tasks in comparison to learning from scratch. Building on top of a given reinforcement learning controller, AdaptNet uses a two-tier hierarchy that augments the original state embedding to support modest changes in a behavior and further modifies the policy network layers to make more substantive changes. The technique is shown to be effective for adapting existing physics-based controllers to a wide range of new styles for locomotion, new task targets, changes in character morphology and extensive changes in environment. Furthermore, it exhibits significant increase in learning efficiency, as indicated by greatly reduced training times when compared to training from scratch or using other approaches that modify existing policies. Code is available athttps://motion-lab.github.io/AdaptNet. 

Heterostyly is a breeding system that promotes outbreeding through a combination of morphological and physiological floral traits. In Turnera these traits are governed by a single, hemizygous S-locus containing just three genes. We report that the S-locus gene, BAHD, is mutated and encodes a severely truncated protein in a self-compatible long homostyle species. Further, a self-compatible long homostyle mutant possesses a T. krapovickasii BAHD allele with a point mutation in a highly conserved domain of BAHD acyl transferases. Wild type and mutant TkBAHD alleles were expressed in Arabidopsis to assay for brassinosteroid (BR) inactivating activity. The wild type but not mutant allele caused dwarfism, consistent with the wild type possessing, but the mutant allele having lost, BR inactivating activity. To investigate whether BRs act directly in self-incompatibility, BRs were added to in vitro pollen cultures of the two mating types. A small morph specific stimulatory effect on pollen tube growth was found with 5 µM brassinolide, but no genotype specific inhibition was observed. These results suggest that BAHD acts pleiotropically to mediate pistil length and physiological mating type through BR inactivation, and that in regard to self-incompatibility, BR acts by differentially regulating gene expression in pistils, rather than directly on pollen. 

Heterostyly distinct hermaphroditic floral morphs enforce outbreeding. Morphs differ structurally, promote cross-pollination, and physiologically block self-fertilization. In Turnera the self-incompatibility (S)-locus controlling heterostyly possesses three genes specific to short-styled morph genomes. Only one gene, TsBAHD, is expressed in pistils and this has been hypothesized to possess brassinosteroid (BR)-inactivating activity. We tested this hypothesis using heterologous expression in Arabidopsis thaliana as a bioassay, thereby assessing growth phenotype, and the impacts on the expression of endogenous genes involved in BR homeostasis and seedling photomorphogenesis. Transgenic A. thaliana expressing TsBAHD displayed phenotypes typical of BR-deficient mutants, with phenotype severity dependent on TsBAHD expression level. BAS1, which encodes an enzyme involved in BR inactivation, was downregulated in TsBAHD-expressing lines. CPD and DWF, which encode enzymes involved in BR biosynthesis, were upregulated. Hypocotyl growth of TsBAHD dwarfs responded to application of brassinolide in light and dark in a manner typical of plants over-expressing genes encoding BR-inactivating activity. These results provide empirical support for the hypothesis that TsBAHD possesses BR-inactivating activity. Further this suggests that style length in Turnera is controlled by the same mechanism (BR inactivation) as that reported for Primula, but using a different class of enzyme. This reveals interesting convergent evolution in a biochemical mechanism to regulate floral form in heterostyly. 

Abstract Background The 29-member Arabidopsis AHL gene family is classified into three main classes based on nucleotide and protein sequence evolutionary differences. These differences include the presence or absence of introns, type and/or number of conserved AT-hook and PPC domains. AHL gene family members are divided into two phylogenetic clades, Clade-A and Clade-B. A majority of the 29 members remain functionally uncharacterized. Furthermore, the biological significance of the DNA and peptide sequence diversity, observed in the conserved motifs and domains found in the different AHL types, is a subject area that remains largely unexplored. Results Transgenic plants overexpressing AtAHL20 flowered later than the wild type under both short and long days. Transcript accumulation analyses showed that 35S:AtAHL20 plants contained reduced FT, TSF, AGL8 and SPL3 mRNA levels. Similarly, overexpression of AtAHL20’s orthologue in Camelina sativa, Arabidopsis’ closely related Brassicaceae family member species, conferred a late-flowering phenotype via suppression of CsFT expression. However, overexpression of an aberrant AtAHL20 gene harboring a missense mutation in the AT-hook domain’s highly conserved R-G-R core motif abolished the late-flowering phenotype. Data from targeted yeast-two-hybrid assays showed that AtAHL20 interacted with itself and several other Clade-A Type-I AHLs which have been previously implicated in flowering-time regulation: AtAHL19, AtAHL22 and AtAHL29. Conclusion We showed via gain-of-function analysis that AtAHL20 is a negative regulator of FT expression, as well as other downstream flowering time regulating genes. A similar outcome in Camelina sativa transgenic plants overexpressing CsAHL20 suggest that this is a conserved function. Our results demonstrate that AtAHL20 acts as a photoperiod-independent negative regulator of transition to flowering. 

Abstract PHYB ACTIVATION TAGGED SUPPRESSOR 1 (BAS1) and SUPPRESSOR OF PHYB‐4 7 (SOB7) are two cytochrome P450 enzymes that inactivate brassinosteroids (BRs) inArabidopsis. The NAC transcription factor (TF) ATAF2 (ANAC081) and the core circadian clock regulator CIRCADIAN CLOCK ASSOCIATED 1 (CCA1) both suppress the expression ofBAS1andSOB7via direct promoter binding. Additionally, BRs cause feedback suppression onATAF2expression. Here, we report that two ATAF‐subgroup TFs, ANAC102 and ATAF1 (ANAC002), also contribute to the transcriptional suppression ofBAS1andSOB7.ANAC102andATAF1gene‐knockout mutants exhibit elevated expression of bothBAS1andSOB7, expanded tissue‐level accumulation of their protein products and reduced hypocotyl growth in response to exogenous BR treatments. Similar toATAF2, bothANAC102andATAF1are transcriptionally suppressed by BRs and white light. NeitherBAS1norSOB7expression is further elevated inATAFdouble or triple mutants, suggesting that the suppression effect of these three ATAFs is not additive. In addition,ATAFsingle, double, and triple mutants have similar levels of BR responsiveness with regard to hypocotyl elongation. ATAF2, ANAC102, ATAF1, and CCA1 physically interact with itself and each other, suggesting that they may coordinately suppressBAS1andSOB7expression via protein–protein interactions. Despite the absence of CCA1‐binding elements in their promoters,ANAC102andATAF1have similar transcript circadian oscillation patterns as that ofCCA1, suggesting that these twoATAFgenes may be indirectly regulated by the circadian clock.