目的:对英文版血液透析患者心理弹性量表（PHRS）进行汉化，并检验其中文版的效度和信度。方法:采用Brislin模式对PHRS进行翻译、回译及跨文化调适，形成中文版PHRS。采用便利抽样法选取2020年9—11月在郑州大学第一附属医院血液净化中心进行血液透析的210例患者进行问卷调查，评价量表信效度。结果:中文版PHRS量表水平的内容效度指数为0.972，条目水平的内容效度指数为0.861～1.000。探索性因子分析共提取4个公因子，累计方差贡献率为68.581%。总量表的Cronbach's α系数为0.912，4个公因子的Cronbach's α系数分别为0.762、0.813、0.889、0.781，重测信度为0.915。中文版PHRS与心理弹性量表（CD-RISC）的相关系数为0.873（ P<0.001）。 结论:中文版PHRS量表具有良好的信效度，可用于我国血液透析患者心理弹性水平的评估。

Inorganic phosphate(Pi)availability is an important factor which affects the growth and yield of crops,thus an appropriate and effective response to Pi fluctuation is critical.However,how crops orches-trate Pi signaling and growth under Pi starvation conditions to optimize the growth defense tradeoff remains unclear.Here we show that a Pi starvation-induced transcription factor NIGT1(NITRATE-INDUCIBLE GARP-TYPE TRANSCRIPTIONAL RE-PRESSOR 1)controls plant growth and prevents a hyper-response to Pi starvation by directly repressing the expression of growth-related and Pi-signaling genes to achieve a balance between growth and response under a varying Pi environ-ment.NIGT1 directly binds to the promoters of Pi starvation signaling marker genes,like IPS1,miR827,and SPX2,under Pi-deficient conditions to mitigate the Pi-starvation responsive(PSR).It also directly represses the expression of vacuolar Pi efflux transporter genes VPE1/2 to regulate plant Pi ho-meostasis.We further demonstrate that NIGT1 con-strains shoot growth by repressing the expression of growth-related regulatory genes,including brassi-nolide signal transduction master regulator BZR1,cell division regulator CYCB1;1,and DNA replication regulator PSF3.Our findings reveal the function of NIGT1 in orchestrating plant growth and Pi starva-tion signaling,and also provide evidence that NIGT1 acts as a safeguard to avoid hyper-response during Pi starvation stress in rice.

SPX-domain-containing proteins (SPXs) play an important role in inorganic phosphate (Pi) sensing,signaling,and transport in eukaryotes.In plants,SPXs are known to integrate cellular Pi status and negatively regulate the activity of Pi central regulators,the PHOSPATE STARVATION RESPONSE proteins (PHRs).The stability of SPXs,such as SPX4,is reduced under Pi-deficient conditions.However,the mechanisms by which SPXs are degraded remain unclear.In this study,using a yeast-two-hybrid screen we identified two RING-finger ubiquitin E3 ligases regulating SPX4 degradation,designated SDEL1 and SDEL2,which were post-transcriptionally induced by Pi starvation.We found that both SDELs were located in the nucleus and cytoplasm,had ubiquitin E3 ligase activity,and directly ubiquitinated the K213 and K299 lysine residues in SPX4 to regulate its stability.Furthermore,we found that PHR2,a Pi central regulator in rice,could compete with SDELs by interacting with SPX4 under Pi-sufficient conditions,which protected SPX4 from ubiquitination and degradation.Consistent with the biochemical function of SDEL1 and SDEL2,overexpression of SDEL1 or SDEL2 resulted in Pi overaccumulation and induced Pi-starvation signaling even under Pi-sufficient conditions.Conversely,their loss-of-function mutants displayed decreased Pi accumulation and reduced Pi-starvation signaling.Collectively,our study revealed that SDEL1 and SDEL2 facilitate the degradation of SPX4 to modulate PHR2 activity and regulate Pi homeostasis and Pi signaling in response to external Pi availability in rice.

Phosphorus is one of mineral elements essential for plant growth and development.To cope with low phosphate (Pi)conditions,plants have evolved complex signaling mecha-nisms including the inositol phosphate (InsP)signaling pathway in which the phosphate starvation response(PHR) transcription factors control the expression of Pi starva-tion-induced genes in a Pi-dependent manner.The activities of PHRs are regulated by their interactions with SPX proteins that act as receptors for inositol pyrophosphates(PP-InsPs),such as InsP7 and InsP8.In plants,the syn-thesis of InsP8 is mediated by the bifunctional kinase/phosphatase enzymes,VIH1 and VIH2.However,InsP6 ki-nases responsible for the synthesis of InsP7 in plants have long remained elusive.

Phosphorous (P) and iron (Fe),two essential nutrients for plant growth and development,are highly abundant elements in the earth's crust but often display low availability to plants.Due to the ability to form insoluble complexes,the antagonistic interaction between P and Fe nutrition in plants has been noticed for decades.However,the underlying molecular mechanism modulating the signaling and homeostasis between them re-mains obscure.Here,we show that the possible iron sensors HRZs,the iron deficiency-induced E3 ligases,could interact with the central regulator of phosphate (Pi) signaling,PHR2,and prompt its ubiquitination at lysine residues K319 and K328,leading to its degradation in rice.Consistent with this,the hrzs mutants dis-played a high Pi accumulation phenotype.Furthermore,we found that iron deficiency could attenuate Pi star-vation signaling by inducing the expression of HRZs,which in turn trigger PHR2 protein degradation.Inter-estingly,on the other hand,rice PHRs could negatively regulate the expression of HRZs to modulate iron deficiency responses.Therefore,PHR2 and HRZs form a reciprocal inhibitory module to coordinate Pi and iron signaling and homeostasis in rice.Taken together,our results uncover a molecular link between Pi and iron master regulators,which fine-tunes plant adaptation to Pi and iron availability in rice.