The ABA receptor PYL9 together with PYL8 plays an important role in regulating lateral root growth

Abstract

Abscisic acid is a phytohormone regulating plant growth, development and stress responses. PYR1/PYL/RCAR proteins are ABA receptors that function by inhibiting PP2Cs to activate SnRK2s, resulting in phosphorylation of ABFs and other effectors of ABA response pathways. Exogenous ABA induces growth quiescence of lateral roots, which is prolonged by knockout of the ABA receptor PYL8. Among the 14 members of PYR1/PYL/RCAR protein family, PYL9 is a close relative of PYL8. Here we show that knockout of both PYL9 and PYL8 resulted in a longer ABA-induced quiescence on lateral root growth and a reduced sensitivity to ABA on primary root growth and lateral root formation compared to knockout of PYL8 alone. Induced overexpression of PYL9 promoted the lateral root elongation in the presence of ABA. The prolonged quiescent phase of the pyl8-1pyl9 double mutant was reversed by exogenous IAA. PYL9 may regulate auxin-responsive genes in vivo through direct interaction with MYB77 and MYB44. Thus, PYL9 and PYL8 are both responsible for recovery of lateral root from ABA inhibition via MYB transcription factors.

Abscisic acid dynamics, signaling, and functions in plants

“…For example, AtPYL6 interacts with and regulates the central JA signaling regulator MYC2 in an ABA‐enhanced manner, which may control the synergistic effects of ABA and JA on the inhibition of seed germination (Aleman et al 2016). AtPYL8 and AtPYL9 interact with the auxin response regulator AtMYB77, which promotes lateral root growth recovery from inhibition by core ABA signaling (Zhao et al 2014; Xing et al 2016). PYLs are differentially expressed in multiple organs, cells, and during different growth stages (Gonzalez‐Guzman et al 2012; Antoni et al 2013).…”

The spatio-temporal specificity of PYR1/PYL/RCAR ABA receptors in response to developmental and environmental cues

“…38 According to the literatures, it is proposed that the dimeric receptors act as the key targets for chemical modulation of vegetative ABA responses as well as the objective receptors for protein engineering, [5][6]39 while the monomeric ones prefer implicated in genetic-modify plant traits for abiotic stress tolerance 2 and also involved in root function regulation. [17][18]23 That the more sensitive of shoot growth than root growth in response to draft stress, is resulted from the insufficient ABA level in the former than the latter to restrict ethylene production. 11 It was shown that leaf ABA concentration ([ABA]) varied greatly as a result of plant growth under different levels of soil water deficit at moderate (60%) or high (90%) relative air humidity (RH).…”

“…21 While PYL8 mediates the ability of ABA to inhibit primary root growth through the PP2C-SnRK2 pathway, 18 it together with PYL9 promotes lateral root growth recovery from inhibition independently of the core signaling pathway by enhancing MYB77-dependent transcription of auxin-responsive genes. 17,23 The cell-specificities of PYR1/PYL/RCAR ABA receptors It has been shown that application ABA directly enhance plasma membrane water permeability of roots cortical cells 15 and guard cells, 24 while inhibit that of vascular bundle-sheath cells 12 and has not effect to that of mesophyll cells. 12,24 The core signaling component SnRK2.6 has been documented implicated in plasma membrane intrinsic proteins PIP2;1 activation through protein phosphorylation at Ser-121, thus increase in guard cell permeability to water.…”

Structural basis for the regulation of phytohormone receptors

“…104) In addition, PYL8 and PYL9 directly interact with MYB44 and MYB77, which are transcription factors that activate multiple auxin-responsive genes to promote lateral root growth. 105,106) Moreover, PYL13 can bind with other PYR/PYL members to antagonize their functions in ABA signaling by inhibiting the formation of a co-receptor complex with PP2Cs. 53,54) ABA signaling is also negatively regulated by the degradation of ABA receptors through ubiquitin-proteasome systems.…”