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Autor(en) / Beteiligte
Titel
Feedback from Lateral Organs Controls Shoot Apical Meristem Growth by Modulating Auxin Transport
Ist Teil von
  • Developmental cell, 2018-01, Vol.44 (2), p.204-216.e6
Ort / Verlag
United States: Elsevier Inc
Erscheinungsjahr
2018
Quelle
Elsevier ScienceDirect Journals Complete
Beschreibungen/Notizen
  • Stem cells must balance self-renewal and differentiation; thus, their activities are precisely controlled. In plants, the control circuits that underlie division and differentiation within meristems have been well studied, but those that underlie feedback on meristems from lateral organs remain largely unknown. Here we show that long-distance auxin transport mediates this feedback in a non-cell-autonomous manner. A low-auxin zone is associated with the shoot apical meristem (SAM) organization center, and auxin levels negatively affect SAM size. Using computational model simulations, we show that auxin transport from lateral organs can inhibit auxin transport from the SAM through an auxin transport switch and thus maintain SAM auxin homeostasis and SAM size. Genetic and microsurgical analyses confirmed the model's predictions. In addition, the model explains temporary change in SAM size of yabby mutants. Our study suggests that the canalization-based auxin flux can be widely adapted as a feedback control mechanism in plants. [Display omitted] •A low-level auxin region exists in the plant shoot apical meristem (SAM)•Auxin level is negatively correlated to the SAM size•Auxin transport from lateral organs inhibits that from the SAM, maintaining SAM size•Auxin transport from branches further triggers changes in SAM size in yab mutants Combining computational simulation and experimental observation of competitive long-distance auxin flows from the plant shoot apical meristem (SAM) and lateral organs, Shi et al. report that lateral organs feed back to SAM stem cells through an auxin transport switch complementary to the local WUS-CLV feedback loop to maintain meristem size.
Sprache
Englisch
Identifikatoren
ISSN: 1534-5807
eISSN: 1878-1551
DOI: 10.1016/j.devcel.2017.12.021
Titel-ID: cdi_hal_primary_oai_HAL_hal_02623655v1

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