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Walker, C. H.

Publications and source records attributed to Walker, C. H..

3 recordsLinked to original sources

Cytokinin signalling regulates two-stage inflorescence arrest in Arabidopsis

To maximise their reproductive success, flowering plants must correctly time their entry into and exit from the reproductive phase (flowering). While much is known about the mechanisms that regulate the initiation of flowering, the regulation of end-of-flowering remains largely uncharacterised. End-of-flowering in Arabidopsis thaliana consists of the quasi-synchronous arrest of individual inflorescences, but it is unclear how this arrest is correctly timed with respect to environmental stimuli and ongoing reproductive success. Here we show that Arabidopsis inflorescence arrest is a complex developmental phenomenon which includes a decline in size and cessation of activity in the inflorescence meristem (IM), coupled with a separable developmental arrest in all unopened floral primordia (floral arrest); these events occur well before the visible arrest of the inflorescence. We show that global removal of inflorescences can delay both IM arrest and floral arrest, but that local fruit removal only delays floral arrest, emphasising the separability of these processes. We test a role for cytokinin in regulating inflorescence arrest, and find that cytokinin treatment can delay arrest. We further show that gain-of-function cytokinin receptor hypersensitive mutants can delay floral arrest, and also IM arrest, depending on the expression pattern of the receptor; conversely, loss-of-function mutants prevent extension of flowering in response to inflorescence removal. Collectively, our data suggest that the dilution of cytokinin among an increasing number of sink organs leads to end-of-flowering in Arabidopsis by triggering IM and floral arrest, conversely meaning that a lack of reproductive success can homeostatically extend flowering in compensation.

plant biology↗

Auxin export from proximal fruits drives arrest in competent inflorescence meristems

A well-defined set of regulatory pathways control entry into the reproductive phase in flowering plants [1]. Conversely, little is known about the mechanisms that control the end of the reproductive phase ( floral arrest), despite this being a critical process for optimising fruit and seed production. Complete fruit removal or lack of fertile fruit-set in male sterile mutants, for example male sterile1 (ms1), prevents timely floral arrest in the model plant Arabidopsis [2]. These observations formed the basis for Hensel and colleagues model in which end-of-flowering was proposed to result from a cumulative fruit/seed-derived signal that caused simultaneous global proliferative arrest (GPA) in all inflorescences [2]. Recent studies have suggested that end-of-flowering involves gene expression changes at the floral meristem which are at least in part controlled by the FRUITFULL-APETELA2 pathway [3,4], however there is limited understanding of how this process is controlled and the communication needed at the whole plant level. Here, we provide new information providing a framework for the fruit-to-meristem (F-M) communication implied by the GPA model [5]. We show that floral arrest in Arabidopsis is not global and does not occur synchronously between branches, but rather that the arrest of each inflorescence is a local process, driven by auxin export from fruit proximal to the inflorescence meristem (IM). Furthermore, we show that inflorescence meristems are only competent for floral arrest once they reach a certain developmental age. Understanding the regulation of floral arrest is of major importance for the future manipulation of flowering to extend and maximise crop yields.

plant biology↗

Root density sensing allows pro-active modulation of shoot growth to avoid future resource limitation

Plants use environmental cues to determine their optimal root and shoot growth. It is well known to gardeners and horticulturists alike that soil volume - most commonly in the form of pot size - strongly restricts plant growth, but the mechanisms by which this effect occurs remain unclear. Here, we show that shoot growth scales directly with soil volume, independently of the nutritional content of the soil, and that plants can become volume restricted even in the presence of abundant resources. We show that plants can detect their soil volume as early as 3 weeks post germination, and that shoot growth restriction therefore constitutes a pro-active decision by the plant to avoid resource limitation later in the life cycle. Shoot growth restriction is not directly linked to root growth restriction, and does not occur in response to the mechanical detection of the pot walls. Rather, we show that plants detect their soil volume by detecting the density of roots in the proximity of their root system. As such, volume restriction may be intimately connected with the mechanism by which plants sense and respond to the roots of other plants in the rhizosphere. Our work demonstrates the remarkable ability of plants to make pro-active decisions about their growth to ensure they can complete their cycle, and has important implications for agricultural practise regarding both nutrient use efficiency and yield.

plant biology↗