Abstract
In plants, aerial organs are initiated at stereotyped intervals, both spatially (every 137° in a pattern called phyllotaxis) and temporally (at prescribed time intervals called plastochrons). To investigate the molecular basis of such regularity, mutants with altered architecture have been isolated. However, most of them only exhibit plastochron defects and/or produce a new, albeit equally reproducible, phyllotactic pattern. This leaves open the question of a molecular control of phyllotaxis regularity. Here, we show that phyllotaxis regularity depends on the function of VIP proteins, components of the RNA polymerase II-associated factor 1 complex (Paf1c). Divergence angles between successive organs along the stem exhibited increased variance in vip3-1 and vip3-2 compared with the wild type, in two different growth conditions. Similar results were obtained with the weak vip3-6 allele and in vip6, a mutant for another Paf1c subunit. Mathematical analysis confirmed that these defects could not be explained solely by plastochron defects. Instead, increased variance in phyllotaxis in vip3 was observed at the meristem and related to defects in spatial patterns of auxin activity. Thus, the regularity of spatial, auxin-dependent, patterning at the meristem requires Paf1c.
Highlights
‘Dreams apart, numerical precision is the very soul of science, and its attainment affords the best, perhaps, the only criterion of the truth of theories and the correctness of experiments’
Aerial organs are initiated from the shoot apical meristem (SAM), where plant stem cells are located, and are called primordia at that stage
If the average plastochron is very small, it can locally reach negative values, and, as organs are initiated before internode grows, a permutation in the sequence of organ emergence is possible. How could this lead to an altered architecture in the end? Let’s take the example of a simple permutation: primordium 3 would emerge before primordium 2 at the meristem; later on, whereas organ 1 would originate from primordium 1, the contiguous organ along the stem would originate from primordium 3 instead of primordium 2, leading to a divergence angle of 137+137=274°
Summary
‘Dreams apart, numerical precision is the very soul of science, and its attainment affords the best, perhaps, the only criterion of the truth of theories and the correctness of experiments’. This is notably the case for mutants with defects in the plastochron, leading to permutations in the final organ positions along the stem: despite the increased variance in divergence angle between fully differentiated organs, primordia are still initiated along the stereotypical 137° divergence angle at the meristem Defective organogenesis has been recorded in severely affected mutants, such as pin-formed 1 ( pin; Gälweiler et al, 1998) or monopteros (mp; Aida et al, 2002), in which no organs are generated These important observations consolidate a role of auxin transport and transduction in organ initiation, and their periodic emergence, they do not formally demonstrate a role of auxin in the spatial regularity of phyllotaxis, notably because of the severity of the mutant phenotypes. We provide evidence that the regularity of the spatial pattern of auxin activity and organ initiation at the SAM requires Paf1c
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