Summary Shoot branching is regulated by multiple signals. Previous studies have indicated that sucrose may promote shoot branching through suppressing the inhibitory effect of the hormone strigolactone (SL). However, the molecular mechanisms underlying this effect are unknown. Here, we used molecular and genetic tools to identify the molecular targets underlying the antagonistic interaction between sucrose and SL. We showed that sucrose antagonizes the suppressive action of SL on tillering in rice and on the degradation of D53, a major target of SL signalling. Sucrose inhibits the gene expression of D3, the orthologue of the Arabidopsis F‐box MAX2 required for SL signalling. Overexpression of D3 antagonizes sucrose inhibition of D53 degradation and enables the SL inhibition of tillering under high sucrose. Sucrose prevents SL‐induced degradation of D14, the SL receptor involved in D53 degradation. In contrast to D3, D14 overexpression enhances D53 protein levels and sucrose‐induced tillering, even in the presence of SL. Our results show that sucrose inhibits SL response by affecting key components of SL signalling and, together with previous studies reporting the inhibition of SL synthesis by nitrate and phosphate, demonstrate the central role played by SLs in the regulation of plant architecture by nutrients.
19Natural selection is a major driver for the origins of adaptations and new species 1 . Whether or 20 not the processes driving adaptation and speciation share a molecular basis remains largely 21 unknown 2 . Here, we show that divergence in hormone signalling contributed to the evolution 22 habits of S. lautus populations, therefore making evolution of the auxin pathway a natural 60 candidate to link the molecular basis of adaptation and speciation. We reasoned that if 61 divergence in the auxin pathway contributed to the evolution of adaptation and speciation in 62 S. lautus, we would discover the following evidence: First, we would detect similar patterns 63 of genetic divergence in auxin-related pathways across multiple erect and prostrate hybrid 64 and natural populations. Second, these populations would differ in phenotypes dependent on 65 auxin, such as their ability to alter the direction of growth in relation to gravity 10,16 . And third, 66 divergence in these auxin-dependent phenotypes would contribute to local adaptation and 67 intrinsic reproductive isolation between populations. 68We test these hypotheses primarily on coastal populations of S. lautus (Fig. 1a, Extended 69Data Table 1), which exhibit strong correlations between growth habit and the environments 70 they occupy 7 . Populations inhabiting sand dunes (Dune hereafter) are erect, while populations 71 growing on adjacent rocky headlands (Headland hereafter) are prostrate ( Fig. 1b). Erect and 72 prostrate growth habits can also be found in related populations from the alpine regions of 73 Australia, with a prostrate population inhabiting an exposed alpine meadow and an erect 74 population inhabiting a sheltered alpine gully (Fig. 1c). Dune populations are continually 75 exposed to high temperatures and sun radiation, low salinity, and low nutrient sand substrate, 76whereas Headland populations are exposed to high salinity, high nutrients and powerful 77 winds 17 . Neighbouring Dune and Headland populations are often sister taxa, group into two 78 major monophyletic clades (eastern and south-eastern) and have evolved their contrasting 79 growth habits independently multiple times 7,20 . These Dune and Headland populations are 80 locally adapted [17][18][19][20] and their F2 hybrids have low fitness 21 , indicating the presence of 81 intrinsic reproductive isolation. Furthermore, performing genetic, physiological, and 82 ecological experimental studies is achievable in this system due to its short life cycle, diploid 83 inheritance, and small vegetative size. Therefore, the Senecio lautus species complex 84The physiological basis of repeated evolution in S. lautus 126Considering we identified a multitude of different auxin related genes between erect and 127 prostrate populations of S. lautus and the regulation and transport of auxin is well established 128 to modulate gravitropism in plants, we predicted that these divergent growth habits may be a 129 direct consequence of changes in the auxin pathway, and can therefore contribute to 130 d...
Plant breeding programs are designed and operated over multiple cycles to systematically change the genetic makeup of plants to achieve improved trait performance for a Target Population of Environments (TPE). Within each cycle, selection applied to the standing genetic variation within a structured reference population of genotypes (RPG) is the primary mechanism by which breeding programs make the desired genetic changes. Selection operates to change the frequencies of the alleles of the genes controlling trait variation within the RPG. The structure of the RPG and the TPE has important implications for the design of optimal breeding strategies. The breeder's equation, together with the quantitative genetic theory behind the equation, informs many of the principles for design of breeding programs. The breeder's equation can take many forms depending on the details of the breeding strategy. Through the genetic changes achieved by selection, the cultivated varieties of crops (cultivars) are improved for use in agriculture. From a breeding perspective, selection for specific trait combinations requires a quantitative link between the effects of the alleles of the genes impacted by selection and the trait phenotypes of plants and their breeding value. This gene-to-phenotype link function provides the G2P map for one to many traits. For complex traits controlled by many genes, the infinitesimal model for trait genetic variation is the dominant G2P model of quantitative genetics. Here we consider motivations and potential benefits of using the hierarchical structure of crop models as CGM-G2P trait link functions in combination with the infinitesimal model for the design and optimisation of selection in breeding programs.
DWARF53 (D53) in rice (Oryza sativa) and its homologs in Arabidopsis (Arabidopsis thaliana), SUPPRESSOR OF MAX2-LIKE 6 (SMXL6), SMXL7 and SMXL8, are well established negative regulators of strigolactone (SL) signalling in shoot branching regulation. Little is known of pea (Pisum sativum) homologs and whether D53 and related SMXLs are specific to SL signalling pathways. Here, we identify two allelic pea mutants, dor-mant3 (dor3), and demonstrate through gene mapping and sequencing that DOR3 corresponds to a homolog of D53 and SMXL6/SMXL7, designated PsSMXL7. Phenotype analysis, gene expression, protein and hormone quantification assays were performed to determine the role of PsSMXL7 in regulation of bud outgrowth and the role of PsSMXL7 and D53 in integrating SL and cytokinin (CK) responses. Like D53 and related SMXLs, we show that PsSMXL7 can be degraded by SL and induces feedback upregulation of PsSMXL7 transcript. Here we reveal a system conserved in pea and rice, whereby CK also upregulates PsSMXL7/D53 transcripts, providing a clear mechanism for SL and CK cross-talk in the regulation of branching. To further deepen our understanding of the branching network in pea, we provide evidence that SL acts via PsSMXL7 to modulate auxin content via PsAFB5, which itself regulates expression of SL biosynthesis genes. We therefore show that PsSMXL7 is key to a triple hormone network involving an auxin-SL feedback mechanism and SL-CK cross-talk.
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