Identification of Players Controlling Meristem Arrest Downstream of the FRUITFULL-APETALA2 Pathway

Martínez-Fernández, Irene; Moura, Stéfanie Menezes de; Alves‐Ferreira, Márcio; Ferrándiz, Cristina; Balanzà, Vicente

doi:10.1104/pp.20.00800

Cited by 20 publications

(35 citation statements)

References 94 publications

(153 reference statements)

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“…In addition to DAM hub, the enhancement of light-mediated CKs signals further negatively regulates ABA content in the dormant bud, indicating that light signal is also involved in the cross-talk between CKs and ABA [123][124][125][126]. It has also been reported that AP2 inhibits meristem activity by negatively regulating CKs signaling, resulting in low mitotic activity and high expression of ABA-responsive genes [127]. Moreover, NAC83-PP2C module and TCP-NCED module indirectly affect the level of CKs by mediating ABA signaling and synthesis pathways, respectively, and jointly regulate corm dormancy in Gladiolus (Figure 3) [27,57].…”

Section: Aba and Cytokininsmentioning

confidence: 98%

ABA and Bud Dormancy in Perennials: Current Knowledge and Future Perspective

Pan

Liang

Sui

et al. 2021

Genes

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Bud dormancy is an evolved trait that confers adaptation to harsh environments, and affects flower differentiation, crop yield and vegetative growth in perennials. ABA is a stress hormone and a major regulator of dormancy. Although the physiology of bud dormancy is complex, several advancements have been achieved in this field recently by using genetics, omics and bioinformatics methods. Here, we review the current knowledge on the role of ABA and environmental signals, as well as the interplay of other hormones and sucrose, in the regulation of this process. We also discuss emerging potential mechanisms in this physiological process, including epigenetic regulation.

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Section: Aba and Cytokininsmentioning

confidence: 98%

ABA and Bud Dormancy in Perennials: Current Knowledge and Future Perspective

Pan

Liang

Sui

et al. 2021

Genes

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“…Certainly, the IM decreases in size and mitotic activity over the course of flowering ( Wang et al, 2020 ; Merelo et al, 2022 ), before undergoing a regulated arrest toward end-of-flowering ( Balanzà et al, 2018 ; Merelo et al, 2022 ), entering a quiescent “dormancy-like” state ( Wuest et al, 2016 ) and then undergoing a gradual senescence ( Wang et al, 2020 ). It is also the case that extending the activity of the IM through genetic manipulations in key regulatory genes such as FRUITFULL can delay overall inflorescence arrest ( Balanzà et al, 2018 ; Martínez-Fernández et al, 2020 ; Merelo et al, 2022 ). However, it is unclear whether the normal end of flower opening in inflorescences is directly caused by IM arrest.…”

Section: Introductionmentioning

confidence: 99%

Cytokinin signaling regulates two-stage inflorescence arrest in Arabidopsis

et al. 2022

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To maximise reproductive success, flowering plants must correctly time entry and exit from the reproductive phase. While much is known about mechanisms that regulate initiation of flowering, end-of-flowering remains largely uncharacterised. End-of-flowering in Arabidopsis (Arabidopsis thaliana) consists of quasi-synchronous arrest of inflorescences, but it is unclear how arrest is correctly timed with respect to environmental stimuli and reproductive success. Here we showed that Arabidopsis inflorescence arrest is a complex developmental phenomenon which includes arrest of the inflorescence meristem (IM), coupled with a separable ‘floral arrest’ of all unopened floral primordia; these events occur well before visible inflorescence arrest. We showed that global inflorescence removal delays both IM and floral arrest, but that local fruit removal only delays floral arrest, emphasising their separability. We tested whether cytokinin regulates inflorescence arrest, and found that cytokinin signaling dynamics mirror IM activity, while cytokinin treatment can delay both IM and floral arrest. We further showed that gain-of-function cytokinin receptor mutants can delay IM and floral arrest; conversely, loss-of-function mutants prevented extension of flowering in response to inflorescence removal. Collectively, our data suggest that dilution of cytokinin among an increasing number of sink organs leads to end-of-flowering in Arabidopsis by triggering IM and floral arrest.

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“…The role of HB21, together with HB40 and HB53, in the maintenance of bud dormancy in Arabidopsis has been previously described in detail (González-Grandío et al, 2017). Interestingly, it has also been suggested that HB21 could be involved in the control of flowering termination participating in inflorescence meristem arrest, which has been proposed to be a type of meristem dormancy (Martínez-Fernández et al, 2020). However, the relevance of HB21 during this developmental process is still unclear.…”

Section: Hb21 Accumulates In the Inflorescence Apex Close To The End ...mentioning

confidence: 98%

“…Recently we have shown that downstream the FUL-AP2 pathway that control the end of flowering process there are some genes involved in the control of bud dormancy . AP2 is a direct repressor of the HB21, and when AP2 is induced in active inflorescence meristems, the expression of HB21, HB53 and in a lesser extent, HB40, are repressed, together with the ABA responses associated to the end of flowering and meristem arrest (Yant et al, 2010;Martínez-Fernández et al, 2020). In this work we have characterized the expression of HB21 during inflorescence development, as well as the contribution of HB21, HB53 and HB40 during the meristem arrest induction at the end of flowering.…”

Section: Introductionmentioning

confidence: 99%

HB21/40/53 promote inflorescence arrest through ABA accumulation at the end of flowering

Sánchez-Gerschon

Ferrándiz

Balanzà

2023

Preprint

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Flowers are produced by the activity of the inflorescence meristem after the floral transition. In plants with indeterminate inflorescences, as Arabidopsis, the final number of flowers produced by the inflorescence meristem will depend on two main factors, the rate of flower production by the meristem and the duration of the phase of inflorescence meristem activity. The end of flowering, understood as the moment when the inflorescence stops the production of new flowers, is associated with the meristem proliferative arrest. At this time point, the meristem ceases to initiate new floral primordia and the unpollinated flowers already formed arrest their development. It has been known for a long time that fruit/seed production induces inflorescence meristem arrest, but the mechanisms controlling this process were elusive. During the last years, the regulation of the end of flowering has started to be elucidated in Arabidopsis. The meristem arrest at the end of flowering is controlled at the genetic level by the FRUITFULL-APETALA2 (FUL-AP2) pathway, that modulates meristem activity. The meristem arrest has been also shown to be controlled at the hormonal level. It has been proposed that auxin could mediate the fruit/seed effect to the meristem. Cytokinins regulation and response have been also proposed as important factors controlling the meristem activity at the end of flowering. Finally, it has been also described that arrested meristems at the end of flowering resembles dormant meristem at the transcriptomic level. Previously, we have shown that the FUL-AP2 pathway controls the expression of the homeodomain leucine zipper transcription factor HOMEOBOX PROTEIN 21 (HB21), a gene involved in the establishment of bud axillary dormancy. In this work we characterize the role of HB21 in the control of the proliferative arrest associated with the end of flowering. We observed that HB21, together with HB40 and HB53, accumulate in the inflorescence apexes at the end of flowering promoting the cessation of inflorescence meristem activity. We also show that HB21 induction of in young apexes is sufficient to induce flower and meristem arrest, likely mediated by an increase in ABA responses. Thus, our work confirms the parallelism proposed between dormant meristems and the arrested meristem at the end of flowering, which appear to be regulated by common pathways, and propose ABA as a new regulator in the control of inflorescence meristem arrest.

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Identification of Players Controlling Meristem Arrest Downstream of the FRUITFULL-APETALA2 Pathway

Cited by 20 publications

References 94 publications

ABA and Bud Dormancy in Perennials: Current Knowledge and Future Perspective

ABA and Bud Dormancy in Perennials: Current Knowledge and Future Perspective

Cytokinin signaling regulates two-stage inflorescence arrest in Arabidopsis

HB21/40/53 promote inflorescence arrest through ABA accumulation at the end of flowering

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