Shoot branching patterns depend on a key developmental decision: whether axillary buds grow out to give a branch or whether they remain dormant in the axils of leaves. This decision is controlled by endogenous and environmental stimuli mediated by hormonal signals. Although genes involved in the long-distance signaling of this process have been identified, the genes responding inside the buds to cause growth arrest remained unknown in Arabidopsis thaliana. Here, we describe an Arabidopsis gene encoding a TCP transcription factor closely related to teosinte branched1 (tb1) from maize (Zea mays), BRANCHED1 (BRC1), which represents a key point at which signals controlling branching are integrated within axillary buds. BRC1 is expressed in developing buds, where it arrests bud development. BRC1 downregulation leads to branch outgrowth. BRC1 responds to developmental and environmental stimuli controlling branching and mediates the response to these stimuli. Mutant and expression analyses suggest that BRC1 is downstream of the MORE AXILLARY GROWTH pathway and that it is required for auxin-induced apical dominance. Therefore, BRC1 acts inside the buds as an integrator of signals controlling bud outgrowth and translates them into a response of cell growth arrest. The conservation of BRC1/tb1 function among distantly related angiosperm species suggests that a single ancestral mechanism of branching control integration evolved before the radiation of flowering plants.

Plants interpret a decrease in the red to far-red light ratio (R:FR) as a sign of impending shading by neighboring vegetation. This triggers a set of developmental responses known as shade avoidance syndrome. One of these responses is reduced branching through suppression of axillary bud outgrowth. The Arabidopsis thaliana gene BRANCHED1 (BRC1), expressed in axillary buds, is required for branch suppression in response to shade. Unlike wild-type plants, brc1 mutants develop several branches after a shade treatment. BRC1 transcription is positively regulated 4 h after exposure to low R:FR. Consistently, BRC1 is negatively regulated by phytochrome B. Transcriptional profiling of wild-type and brc1 buds of plants treated with simulated shade has revealed groups of genes whose mRNA levels are dependent on BRC1, among them a set of upregulated abscisic acid response genes and two networks of cell cycle– and ribosome-related downregulated genes. The downregulated genes have promoters enriched in TEOSINTE BRANCHED1, CYCLOIDEA, and PCF (TCP) binding sites, suggesting that they could be transcriptionally regulated by TCP factors. Some of these genes respond to BRC1 in seedlings and buds, supporting their close relationship with BRC1 activity. This response may allow the rapid adaptation of plants to fluctuations in the ratio of R:FR light.

Faithful inheritance of eukaryotic genomes requires the orchestrated activation of multiple DNA replication origins (ORIs). Although origin firing is mechanistically conserved, how origins are specified and selected for activation varies across different model systems. Here, we provide a complete analysis of the nucleosomal landscape and replication program of the human parasite Leishmania major, building on a better evolutionary understanding of replication organization in Eukarya. We found that active transcription is a driving force for the nucleosomal organization of the L. major genome and that both the spatial and the temporal program of DNA replication can be explained as associated to RNA polymerase kinetics. This simple scenario likely provides flexibility and robustness to deal with the environmental changes that impose alterations in the genetic programs during parasitic life cycle stages. Our findings also suggest that coupling replication initiation to transcription elongation could be an ancient solution used by eukaryotic cells for origin maintenance.