缺血后适应对局灶性脑缺血/再灌注大鼠p38表达的影响

目的：探讨缺血后适应对大鼠局灶性脑缺血/再灌注损伤后p38表达的影响。方法：将30只雄性SD大鼠随机分为3组（n=10）：假手术组（sham组）、缺血/再灌注（I/R）组和缺血后适应（IP）组。利用TUNEL法观察神经细胞凋亡的变化,应用Westernblot检测大鼠局灶性脑I/R损伤后p38蛋白表达水平的变化。结果：大鼠脑缺血/再灌注后凋亡细胞数量和p38蛋白表达水平均显著升高,而IP组凋亡细胞数量和p38蛋白表达水平均显著低于IR组（P〈0.01）。结论：缺血后适应可抑制大鼠脑缺血/再灌注后细胞凋亡的发生,此作用可能与下调p38蛋白表达有关。     

瘦素对小鼠脑缺血/再灌注损伤神经元凋亡的影响

目的：研究Leptin在脑缺血性损伤神经元凋亡中的作用及其机制。方法：将75只雄性昆明小鼠完全随机分成3组,即假手术组、缺血/再灌注模型组、Leptin干预组;通过大脑中动脉栓塞（MCAO）复制小鼠局灶性脑缺血再灌注损伤模型,Leptin干预组在缺血0 min腹腔注射Leptin（1μg/g体重）,TUNEL染色检测神经元凋亡,RT-PCR检测凋亡相关基因bcl-2和caspase-3 mRNA表达,免疫组化凋亡相关基因bcl-2和caspase-3蛋白水平的表达。结果：模型组脑缺血中心区神经元以坏死为主,与假手术组相比,其半影区神经元凋亡数量显著增多、促凋亡基因cas-pase-3和抑凋亡基因bcl-2的mRNA和蛋白表达水平均显著升高（P<0.01）;与模型组比较,Leptin干预组半影区凋亡神经元数量显著减少、caspase-3 mRNA和蛋白表达水平显著降低（P<0.01）,抑凋亡基因bcl-2 mRNA和蛋白表达水平显著升高（P<0.01）。结论：Leptin能够通过上调抑凋亡基因bcl-2表达,下调促凋亡基因caspase-3表达抑制神经元凋亡,在脑缺血性损伤中发挥神经保护作用。     

异丙酚对局灶性脑缺血／再灌注星形胶质细胞GFAP表达的影响

目的：探讨异丙酚对局灶性脑缺血／再灌注后星形胶质细胞胶质纤维酸性蛋白（GFAP）表达的影响。方法：大脑中动脉插线法制作大鼠局灶性脑缺血／再灌注模型。观察脑缺血2h再灌注24h后神经功能损害改变并评分,并采用免疫荧光组织化学法检测大鼠齿状回GFAP蛋白的表达。结果：缺血／再灌注后可诱导大鼠齿状回GFAP表达明显增强,异丙酚可抑制缺血／再灌注后GFAP的表达,明显改善大鼠神经功能损害（P〈0．05或0.01）。结论：异丙酚通过抑制脑缺血后星形胶质细胞GFAP的过度表达发挥抗脑缺血损伤保护神经元作用。     

PEP-1超氧化物歧化酶对大鼠脑缺血再灌注后Bcl-2的影响

目的：观察细胞穿透肽-铜,锌超氧化物歧化酶（PEP-1-SOD1）预处理对大鼠局灶性脑缺血再灌注损伤的改善作用及其脑保护机制。方法：线栓法建立大鼠局灶性脑缺血6h后再灌注损伤模型,进行神经行为评分,并通过HE染色在光镜下观察神经细胞损伤变化,免疫组化法检测B细胞淋巴瘤基因-2（B—celllymphoma-2,Bcl-2）蛋白的阳性表达。结果：盐水对照组（缺血再灌注组或模型组）神经障碍显著高于假手术组（P〈0．05）,与模型组相比,PEP-1-SOD1预处理组可降低神经障碍评分（P〈0．05）;光镜下,假手术组神经细胞结构正常,PEP-1-SDO1预处理组和缺血再灌注组均有不同程度的缺血再灌注损伤,PEP-1-SOD1预处理组较缺血再灌注组损伤轻;假手术组Bcl-2蛋白表达极弱,缺血再灌注组和PEP-1-SOD1预处理组在脑缺血再灌注后6h在缺血半暗带周围出现Bcl-2蛋白阳性表达,24h达到高峰,48h表达开始减少。与假手术组相比,PEP-1-SOD1预处理组和缺血再灌注组Bcl-2蛋白阳性细胞数显著增多（P〈0．05）;与缺血再灌注组相比,PEP-1-SOD1预处理组Bcl-2蛋白阳性细胞数显著增多（P〈0．05）。结论：PEP-1-SOD1对大鼠局灶性脑缺血再灌注损伤有保护作用,PEP-1-SOD1可通过上调Bcl-2蛋白的表达发挥脑保护作用。     

参芎注射液对脑缺血再灌注大鼠的神经元保护作用

目的:观察参芎注射液对大鼠局灶性脑缺血再灌注后神经细胞凋亡及内质网应激相关因子葡萄糖调节蛋白/免疫球蛋白结合蛋白(GRP78/Bip)表达的影响.方法:100只雄性SD大鼠随机分为正常组、假手术组、脑缺血再灌注组、参芎治疗组;后两组根据再灌注时间不同各分为6、12、24、72 h四个亚组;采用大鼠大脑中动脉线栓法制备局灶性脑缺血再灌注模型.TUNEL法观察细胞凋亡情况;免疫组化和RT-PCR法检测各实验组中缺血周围区GRP78/Bip的表达.结果:TUNEL法表明参芎治疗组大鼠大脑神经细胞凋亡程度较缺血再灌注组明显减轻.免疫组化和RT-PCR检测均发现各时间点缺血再灌注组大鼠GRP78/Bip表达高于假手术组及正常组;脑缺血再灌注组及参芎治疗组GRP78/Bip的表达于缺血后12 h最高,72 h恢复至正常水平,且均呈现先升高后降低的趋势;各时间点缺血再灌注组GRP78/Bip表达均高于参芎治疗组.结论:再灌注损伤后12 h内出现GRP78/Bip表达升高.参芎注射液可以下调其表达,从而可能通过减轻内质网应激而减轻缺血再灌注损伤起到神经元保护的作用.     

促红细胞生成素对大鼠局灶性脑缺血再灌注神经元的保护作用及P53蛋白的表达

目的:探讨促红细胞生成素(Epo)对大鼠局灶性脑缺血再灌注神经细胞的保护作用.方法:60只SD大鼠随机分为缺血再灌注Epo治疗组(又分为高剂量A组、低剂量B组)、缺血再灌注组(C组)及假手术组(D组),采用大脑中动脉线栓法制备大鼠局灶性脑缺血再灌注模型.参考Longa的5分制法在大鼠麻醉清醒后进行评分,TTC染色法观察线栓侧的梗死体积,并检测脑组织含水量的变化,HE染色法观察脑缺血再灌注后脑组织的病理变化,TUNEL法观察神经细胞凋亡情况,western blot法观察p53蛋白的表达变化.结果:对照组比较,大鼠脑缺血再灌注后出现不同程度的脑梗死,24h后缺血中心区及周围区均可见到p53蛋白表达.缺血再灌注6h内给予Epo可显著改善大鼠神经功能评分,减少梗死体积及脑组织含水量,减轻病理学变化及神经细胞凋亡.结论:Epo通过调控神经细胞凋亡、改善缺血再灌注损伤而发挥脑保护作用,P53蛋白参与缺血再灌注后神经细胞凋亡机制.     

UCF-101对大鼠局灶性脑缺血再灌注后JNK和ERK活性的影响

目的:探讨UCF-101对局灶性脑缺血再灌注大鼠脑内c-Jun氨基末端激酶(JNK)和胞外信号调节酶(ERK)活性的影响,进一步探讨UCF-101对局灶性脑缺血再灌注损伤脑保护作用的机制。方法:采用大脑中动脉线栓法(MCAO)建立大鼠局灶性脑缺血再灌注模型,随机分为假手术组,缺血再灌注组,UCF组,应用TTC检测大鼠脑梗死体积,TUNEL法检测神经元凋亡,Western blot检测ERK和JNK的活性。结果:UCF-101可下调脑缺血再灌注大鼠脑组织JNK蛋白的活性,上调ERK蛋白的活性,并降低梗死体积、坏死和凋亡细胞数。结论:UCF-101对大鼠局灶性脑缺血再灌注损伤有保护作用,抑制JNK凋亡通路、促进ERK生存通路,从而减轻细胞凋亡是其脑保护机制之一。     

电针对局灶脑缺血/再灌注模型大鼠大脑缺血皮质区P2X7R与NLRP3炎性小体表达的影响

目的观察电针治疗对局灶脑缺血/再灌注模型大鼠大脑缺血皮质区嘌呤受体配体门控性离子通道7(purinergic2X7 receptor,P2X7R)和Nod样受体蛋白3(NOD-like receptor pyrin 3,NLRP3)炎性小体表达的影响,探讨电针治疗减轻局灶脑缺血/再灌注炎性损伤的可能机制。方法雄性SD大鼠随机分为假手术组、模型组、电针组,每组16只。采用改良线栓法制备局灶脑缺血/再灌注模型。以大鼠"百会"、"合谷"和"太冲"为电针穴位。采用Bederson行为学评分评价各组大鼠神经功能缺损程度,Western blot和RT-q PCR检测大脑缺血皮区P2X7R、NLRP3蛋白及m RNA表达情况,ELISA检测脑内IL-1β和IL-18含量,荧光共聚焦显微镜检测脑内Iba-1阳性小胶质细胞数量。结果脑缺血再灌注后24h,电针治疗可明显改善神经功能缺损症状。RT-q PCR和Western blot检测显示,模型组大脑皮质缺血区P2X7R和NLRP3 m RNA和蛋白表达较假手术组明显升高,电针治疗可明显减少脑缺血再灌注后P2X7R和NLRP3 m RNA和蛋白表达的升高。ELISA测定表明,与模型组相比,电针组大脑皮质缺血区IL-1β和IL-18含量明显降低。激光扫描共聚焦显微镜观察发现,脑缺血再灌注后24h,电针治疗可明显减少大脑皮质缺血区Iba-1阳性小胶质细胞数量。结论电针可抑制局灶脑缺血/再灌注模型大鼠脑内P2X7R、NLRP3表达的上调,削弱小胶质细胞激活,减轻炎症因子分泌,从而减轻脑缺血/再灌注炎性损伤。     

甘珀酸干预对大鼠脑缺血再灌注损伤的影响

目的观察缝隙连接阻断剂甘珀酸对局灶性脑缺血/再灌注损伤的影响。方法采用大鼠大脑中动脉阻塞再灌流模型（MCAO）,将动物随机分为脑缺血60min再灌注（MCAO）组,脑缺血再灌注加甘珀酸干预（MCAO＋CBX）组和假手术组（sham）。采用尼氏染色显示脑梗死灶并计算梗死灶体积;应用免疫荧光与TUNEL染色法分别观察脑缺血后3d与7d不同时间点缺血边缘区胶质纤维酸性蛋白（GFAP）的表达和细胞凋亡情况。结果（1）缺血后3d、7d MCAO＋CBX组大鼠梗死体积小于MCAO组,3d、7d MCAO＋CBX组大鼠梗死体积较MCAO组分别缩小5%和4.6%;（2）缺血后3d、7d于缺血边缘区可见大量TUNEL阳性染色细胞,且MCAO组大鼠缺血边缘区细胞凋亡数目明显多于MCAO＋CBX大鼠（P〈0.001）;（3）缺血后3d和7d组缺血边缘区GFAP表达明显增强,3d的MCAO组与MCAO＋CBX组大鼠缺血边缘区GFAP的表达均较假手术组强（P〈0.05）,7d的MCAO＋CBX组大鼠缺血边缘区GFAP的表达较假手术组强（P〈0.001）,但明显弱于MCAO组大鼠（P〈0.01）;结论缝隙连接阻断剂甘珀酸可减少大鼠大脑中动脉阻塞后脑梗死体积,其机制可能与阻断缝隙连接后缺血边缘区神经元凋亡降低有关,星型胶质细胞的反应性变化参与了该过程。     

脑缺血和缺血再灌注大鼠皮层神经元自噬的动态变化

目的：探讨脑缺血和缺血/再灌注不同时间大鼠大脑皮层神经元自噬的变化。方法：健康雄性SD大鼠60只,随机分为：假手术（Sham）组（n=10）,脑缺血和缺血/再灌注模型组（n=50）.模型组分别在缺血30min、2h,缺血2h再灌注1h、6h、24h五个时间点,随机抽取10只大鼠,测定脑梗死体积和脑含水量,同时采用Western印迹法测定各组大鼠大脑皮层中微管相关蛋白轻链3-Ⅱ（LC3-Ⅱ）的水平,透射电镜检测大脑皮层神经细胞自噬情况。结果：脑缺血30min时LC3-Ⅱ/Ⅰ比值未见明显上升,缺血2h时LC3-Ⅱ/Ⅰ比值开始升高,明显高于Sham组（P<0.01）;缺血/再灌注1h、6h时LC3-Ⅱ/Ⅰ比值虽较缺血2h组有所下降,但仍明显高于Sham组（P<0.05）;缺血/再灌注24h时LC3Ⅱ/Ⅰ比值达高峰,明显高于Sham组（P<0.01）。透射电镜观察进一步证实该现象。缺血/再灌注6h和24h时大鼠脑梗死体积明显增加,与Sham组比较有统计学差异（P<0.01）。缺血/再灌注24h大鼠脑组织含水量明显增加,明显高于Sham组（P<0.05）。HE染色显示：仅在缺血/再灌注24h组大鼠皮层见组织水肿、疏松,部分细胞变性、凋亡,海马区见大量神经元细胞核皱缩、深染呈变性凋亡状。结论：局灶性脑缺血和缺血/再灌注模型中大脑皮层缺血2 h神经元自噬即明显激活,缺血/再灌注1 h、6 h自噬均持续增高,缺血/再灌注24 h自噬达高峰。     

姜黄素对大鼠脑缺氧缺血损伤时脑组织MDA变化、caspase-3表达及细胞凋亡的影响

目的:探讨姜黄素对大鼠脑缺氧缺血损伤时脑组织MDA变化、caspase-3表达及细胞凋亡的影响。方法:健康SD雄性大鼠48只,随机分为假手术对照组(SH组)、脑缺氧缺血组(HI组)、姜黄素组(CU组)、溶剂对照组(SC组);生化方法检测脑组织丙二醛(MDA)含量;免疫组织化学测定大脑皮质caspase-3的表达;电镜观察大脑皮质形态学结构变化。结果:姜黄素可使脑组织MDA含量明显减低,并且抑制caspase-3蛋白的表达;神经元细胞凋亡减轻。结论:细胞凋亡参与了大脑缺氧缺血损伤的发生,姜黄素可能通过减低MDA含量、下调caspase-3的表达抑制细胞凋亡,从而减轻脑缺氧缺血性损伤。     

Cell Wall,Cytoskeleton, and Cell Expansion in Higher Plants

To accommodate two seemingly contradictory biological roles in plant physiology, providing both the rigid structural support of plant cells and the adjustable elasticity needed for cell expansion, the composition of the plant cell wall has evolved to become an intricate network of cellulosic, hemicellulosic, and pectic polysaccharides and protein. Due to its complexity, many aspects of the cell wall influence plant cell expansion, and many new and insightful observations and technologies are forthcoming. The biosynthesis of cell wall polymers and the roles of the variety of proteins involved in polysaccharide synthesis continue to be characterized. The interactions within the cell wall polymer network and the modification of these interactions provide insight into how the plant cell wall provides its dual function. The complex cell wall architecture is controlled and organized in part by the dynamic intracellular cytoskeleton and by diverse trafficking pathways of the cell wall polymers and cell wall-related machinery. Meanwhile, the cell wall is continually influenced by hormonal and integrity sensing stimuli that are perceived by the cell. These many processes cooperate to construct, maintain, and manipulate the intricate plant cell wall--an essential structure for the sustaining of the plant stature, growth, and life.     

Salt Stress in Arabidopsis： Lipid Transfer Protein AZI1 and Its Control by Mitogen-Activated Protein Kinase MPK3

A plant＇s capability to cope with environmental challenges largely relies on signal transmission through mitogen-activated protein kinase （MAPK） cascades. In Arabidopsis thaliana, MPK3 is particularly strongly associated with numerous abiotic and biotic stress responses. Identification of MPK3 substrates is a milestone towards improving stress resistance in plants. Here, we characterize AZI1, a lipid transfer protein （LTP）-related hybrid proline-rich protein （HyPRP）, as a novel target of MPK3. AZI1 is phosphorylated by MPK3 in vitro. As documented by co-immunoprecipitation and bimolecular fluorescence complementation experiments, AZI1 interacts with MPK3 to form protein complexes in planta. Furthermore, null mutants of azil are hypersensitive to salt stress, while AZIl-overexpressing lines are markedly more tolerant. AZI1 overexpression in the mpk3 genetic background partially alleviates the salt-hypersensitive phenotype of this mutant, but functional MPK3 appears to be required for the full extent of AZIl-conferred robustness. Notably, this robustness does not come at the expense of normal development. Immunoblot and RT-PCR data point to a role of MPK3 as positive regulator of AZI1 abundance.     

Emerging roles of miR-210 and other non-coding RNAs in the hypoxic response

Hypoxia is a key component of the tumor microenviron- merit and represents a well-documented source of thera- peutic failure in clinical oncology. Recent work has provided support for the idea that non-coding RNAs, and in particular, microRNAs, may play important roles in the adaptive response to low oxygen in tumors. Specifically, all published studies agree that the induction of microRNA- 210 （miR-210） is a consistent feature of the hypoxic re- sponse in both normal and malignant cells, miR-210 is a robust target of hypoxia-inducible factors, and its overex- pression has been detected in a variety of diseases with a hypoxic component, including most solid tumors. High levels of miR-210 have been linked to an in vivo hypoxic sig- nature and to adverse prognosis in breast and pancreatic cancer patients. A wide variety of miR-210 targets have been identified, pointing to roles in mitochondrial metabol- ism, angiogenesis, DNA damage response, apoptosis, and cell survival. Such targets are suspected to affect the devel- opment of tumors in multiple ways; therefore, an increased knowledge about miR-210＇s functions may lead to novel diagnostic and therapeutic approaches in cancer.     

Organelle pH in the Arabidopsis Endomembrane System

The pH of intracellular compartments is essential for the viability of cells. Despite its relevance, little is known about the pH of these compartments. To measure pH in vivo, we have first generated two pH sensors by combining the improved-solubility feature of solubility-modified green fluorescent protein （GFP） （smGFP） with the pH-sensing capabil- ity of the pHluorins and codon optimized for expression in Arabidopsis. PEpHluorin （plant-solubility-modified ecliptic pHluorin） gradually loses fluorescence as pH is lowered with fluorescence vanishing at pH 6.2 and PRpHluorin （plant- solubility-modified ratiomatric pHluorin）, a dual-excitation sensor, allowing for precise measurements. Compartment- specific sensors were generated by further fusing specific sorting signals to PEpHluorin and PRpHluorin. Our results show that the pH of cytosol and nucleus is similar （pH 7.3 and 7.2）, while peroxisomes, mitochondrial matrix, and plastidial stroma have alkaline pH. Compartments of the secretory pathway reveal a gradual acidification, spanning from pH 7.1 in the endoplasmic reticulum （ER） to pH 5.2 in the vacuole. Surprisingly, pH in the trans-Golgi network （TGN） and mul- tivesicular body （MVB） is, with pH 6.3 and 6.2, quite similar. The inhibition of vacuolar-type H＋-ATPase （V-ATPase） with concanamycin A （ConcA） caused drastic increase in pH in TGN and vacuole. Overall, the PEpHluorin and PRpHluorin are excellent pH sensors for visualization and quantification of pH in vivo, respectively.     

Dissecting the Heat Stress Response in Chlamydomonas by Pharmaceutical and RNAi Approaches Reveals Conserved and Novel Aspects

To study how conserved fundamental concepts of the heat stress response （HSR） are in photosynthetic eukaryotes, we applied pharmaceutical and antisense/amiRNA approaches to the unicellular green alga Chlamydomonas reinhardtii. The Chlamydomonas HSR appears to be triggered by the accumulation of unfolded proteins, as it was induced at ambient temperatures by feeding cells with the arginine analog canavanine. The protein kinase inhibitor staurosporine strongly retarded the HSR, demonstrating the importance of phosphorylation during activation of the HSR also in Chlamydomonas. While the removal of extracellular calcium by the application of EGTA and BAPTA inhibited the HSR in moss and higher plants, only the addition of BAPTA, but not of EGTA, retarded the HSR and impaired thermotoler- ance in Chlamydomonas. The addition of cycloheximide, an inhibitor of cytosolic protein synthesis, abolished the attenu- ation of the HSR, indicating that protein synthesis is necessary to restore proteostasis. HSP90 inhibitors induced a stress response when added at ambient conditions and retarded attenuation of the HSR at elevated temperatures. In addition, we detected a direct physical interaction between cytosolic HSP90A/HSP70A and heat shock factor 1, but surprisingly this interaction persisted after the onset of stress. Finally, the expression of antisense constructs targeting chloroplast HSP70B resulted in a delay of the cell＇s entire HSR, thus suggesting the existence of a retrograde stress signaling cascade that is desensitized in HSP7OB-antisense strains.     

Strigolactone-Regulated Hypocotyl Elongation Is Dependent on Cryptochrome and Phytochrome Signaling Pathways in Arabidopsis

Seedling development including hypocotyl elongation is a critical phase in the plant life cycle. Light regula- tion of hypocotyl elongation is primarily mediated through the blue light photoreceptor cryptochrome and red/far-red light photoreceptor phytochrome signaling pathways, comprising regulators including COP1, HY5, and phytochrome- interacting factors （PIFs）. The novel phytohormones, strigolactones, also participate in regulating hypocotyl growth. However, how strigolactone coordinates with light and photoreceptors in the regulation of hypocotyl elongation is largely unclear. Here, we demonstrate that strigolactone inhibition of hypocotyl elongation is dependent on cryp- tochrome and phytochrome signaling pathways. The photoreceptor mutants cry1 cry2, phyA, and phyB are hyposensi- tive to strigolactone analog GR24 under the respective monochromatic light conditions, while cop1 and pifl pif3 pif4 pif5 （pifq） quadruple mutants are hypersensitive to GR24 in darkness. Genetic studies indicate that the enhanced respon- siveness of cop1 to GR24 is dependent on HY5 and MAX2, while that of pifq is independent of HY5. Further studies demonstrate that GR24 constitutively up-regulates HY5 expression in the dark and light, whereas GR24-promoted HY5 protein accumulation is light- and cryptochrome and phytochrome photoreceptor-dependent. These results suggest that the light dependency of strigolactone regulation of hypocotyl elongation is likely mediated through MAX2-dependent promotion of HY5 expression, light-dependent accumulation of HY5, and PIF-regulated components.     

Regulation of Cytokinesis by Exocyst Subunit SEC6 and KEULE in Arabidopsis thaliana

Proper vesicle tethering and membrane fusion at the cell plate are essential for cytokinesis. Both the vesicle tethering complex exocyst and membrane fusion regulator KEULE were shown to function in cell plate formation, but the exact mechanisms still remain to be explored. In this study, using yeast two-hybrid （Y-2-H） assay, we found that SEC6 interacted with KEULE, and that a small portion of C-terminal region of KEULE was required for the interaction. The direct SEC6-KEULE interaction was supported by further studies using in vitro pull-down assay, immunoprecipitation, and in vivo bimolecular florescence complementation （BIFC） microscopy, sec6 mutants were male gametophytic lethal as reported; however, pollen-rescued sec6 mutants （PRsec6） displayed cytokinesis defects in the embryonic cells and later in the leaf pavement cells and the guard cells. SEC6 and KEULE proteins were co-localized to the cell plate during cytokine- sis in transgenic Arabidopsis. Furthermore, only SEC6 but not other exocyst subunits located in the cell plate interacted with KEULE in vitro. These results demonstrated that, like KEULE, SEC6 plays a physiological role in cytokinesis, and the SEC6-KEULE interaction may serve as a novel molecular linkage between arriving vesicles and membrane fusion machin- ery or directly regulate membrane fusion during cell plate formation in plants.     

Perturbation of Auxin Homeostasis Caused by Mitochondrial FtSH4 Gene-Mediated Peroxidase Accumulation Regulates Arabiclopsis Architecture

Reactive oxygen species and auxin play important roles in the networks that regulate plant development and morphogenetic changes, However, the molecular mechanisms underlying the interactions between them are poorly understood. This study isolated a mas （More Axillary Shoots） mutant, which was identified as an allele of the mitochondrial AAA-protease AtFtSH4, and characterized the function of the FtSH4 gene in regulating plant development by medi- ating the peroxidase-dependent interplay between hydrogen peroxide （H2Oz） and auxin homeostasis. The phenotypes of dwarfism and increased axillary branches observed in the mas （renamed as ftsh4-4） mutant result from a decrease in the IAA concentration. The expression levels of several auxin signaling genes, including IAA1, IAA2, and IAA3, as well as several auxin binding and transport genes, decreased significantly in ftsh4-4 plants. However, the H202 and peroxidases levels, which also have IAA oxidase activity, were significantly elevated in ftsh4-4 plants. The ftsh4-4 phenotypes could be reversed by expressing the iaaM gene or by knocking down the peroxidase genes PRX34 and PRX33. Both approaches can increase auxin levels in the ftsh4-4 mutant. Taken together, these results provided direct molecular and genetic evidence for the interaction between mitochondrial ATP-dependent protease, H2O2, and auxin homeostasis to regulate plant growth and development.