Wheat zinc finger protein TaLSD1, a negative regulator of programmed cell death, is involved in wheat resistance against stripe rust fungus

2013 ◽  
Vol 71 ◽  
pp. 164-172 ◽  
Author(s):  
Jun Guo ◽  
Pengfei Bai ◽  
Qian Yang ◽  
Furong Liu ◽  
Xiaodong Wang ◽  
...  
2020 ◽  
Vol 104 ◽  
pp. 103542 ◽  
Author(s):  
Muhammad Nadeem Abbas ◽  
Hanghua Liang ◽  
Saima Kausar ◽  
Zhen Dong ◽  
Hongjuan Cui

2001 ◽  
Vol 21 (8) ◽  
pp. 2880-2890 ◽  
Author(s):  
Madeleine J. Meagher ◽  
Robert E. Braun

ABSTRACT The transition from preimplantation to postimplantation development leads to the initiation of complex cellular differentiation and morphogenetic movements, a dramatic decrease in cell cycle length, and a commensurate increase in the size of the embryo. Accompanying these changes is the need for the transfer of nutrients from the mother to the embryo and the elaboration of sophisticated genetic networks that monitor genomic integrity and the homeostatic control of cellular growth, differentiation, and programmed cell death. To determine the function of the murine zinc finger protein ZFR in these events, we generated mice carrying a null mutation in the gene encoding it. Homozygous mutant embryos form normal-appearing blastocysts that implant and initiate the process of gastrulation. Mutant embryos form mesoderm but they are delayed in their development and fail to form normal anterior embryonic structures. Loss of ZFR function leads to both an increase in programmed cell death and a decrease in mitotic index, especially in the region of the distal tip of the embryonic ectoderm. Mutant embryos also have an apparent reduction in apical vacuoles in the columnar visceral endoderm cells in the extraembryonic region. Together, these cellular phenotypes lead to a dramatic development delay and embryonic death by 8 to 9 days of gestation, which are independent of p53 function.


2015 ◽  
Vol 156 (3) ◽  
pp. 262-277 ◽  
Author(s):  
Mohamed Awaad Abou-Attia ◽  
Xiaojie Wang ◽  
Mohamed Nashaat Al-Attala ◽  
Qiang Xu ◽  
Gangming Zhan ◽  
...  

2013 ◽  
Vol 35 (6) ◽  
pp. 1863-1871 ◽  
Author(s):  
Muhammad Kamran Qureshi ◽  
Neerakkal Sujeeth ◽  
Tsanko S. Gechev ◽  
Jacques Hille

Genetics ◽  
2007 ◽  
Vol 175 (4) ◽  
pp. 1719-1733 ◽  
Author(s):  
Peter W. Reddien ◽  
Erik C. Andersen ◽  
Michael C. Huang ◽  
H. Robert Horvitz

2011 ◽  
Vol 24 (1) ◽  
pp. 79-90 ◽  
Author(s):  
Xiaojie Wang ◽  
Chunlei Tang ◽  
Hongchang Zhang ◽  
Jin-Rong Xu ◽  
Bo Liu ◽  
...  

Defender against cell death (DAD) genes are known to function as negative regulators of cell death in animals. In plants, DAD orthologs are conserved but their role in cell death regulation is not well understood. Here, we report the characterization of the TaDAD2 gene in wheat. The predicted amino acid sequence of TaDAD2 contains typical structural features of DAD proteins, including a signal peptide, three transmembrane regions, and a subunit of oligosaccharyltransferase. Transcripts of TaDAD2 were detected in wheat leaves, culms, roots, florets, and spikelets. The expression level of TaDAD2 was reduced in the initial contact with the stripe rust fungus, subsequently induced and peaked at 18 h postinoculation (hpi), gradually reduced at 24 to 48 hpi, and restored to control level at 72 to 120 hpi. In addition, TaDAD2 exhibited positive transcriptional responses to abiotic stresses after the initial reduction at 1 hpi. Overexpression of TaDAD2 in tobacco leaves inhibited cell death. Furthermore, knocking down TaDAD2 expression by virus-induced gene silencing enhanced the susceptibility of wheat cv. Suwon11 to avirulent race CYR23 and reduced necrotic area at the infection sites. These results indicate that TaDAD2 may function as a suppressor of cell death in the early stages of wheat–stripe rust fungus interaction. However, it is dispensable for or plays an opposite role in hypersensitive response or cell death triggered by an avirulent race of stripe rust fungus at late-infection stages.


Cell ◽  
1997 ◽  
Vol 88 (5) ◽  
pp. 685-694 ◽  
Author(s):  
Robert A Dietrich ◽  
Michael H Richberg ◽  
Renate Schmidt ◽  
Caroline Dean ◽  
Jeffery L Dangl

2021 ◽  
Author(s):  
Pengxiang Chen ◽  
Fang Zhi ◽  
Xuewei Li ◽  
Wenyun Shen ◽  
Mingjia Yan ◽  
...  

Abstract Water deficit is one of the main challenges for apple (Malus × domestica) growth and productivity. Breeding drought-tolerant cultivars depends on a thorough understanding of the drought responses of apple trees. Here, we identified the zinc-finger protein B-BOX 7/CONSTANS-LIKE 9 (MdBBX7/MdCOL9), which plays a positive role in apple drought tolerance. The overexpression of MdBBX7 enhanced drought tolerance, whereas knocking down MdBBX7 expression reduced it. Chromatin immunoprecipitation-sequencing (ChIP-seq) analysis identified one cis-element of MdBBX7, CCTTG, as well as its known binding motif, the T/G box. ChIP-seq and RNA-seq identified 1,197 direct targets of MdBBX7, including ETHYLENE RESPONSE FACTOR (ERF1), EARLY RESPONSIVE TO DEHYDRATION 15 (ERD15), and GOLDEN2-LIKE 1 (GLK1) and these were further verified by ChIP-qPCR and electronic mobility shift assays. Yeast two-hybrid screen identified an interacting protein of MdBBX7, RING-type E3 ligase MYB30-INTERACTING E3 LIGASE 1 (MIEL1). Further examination revealed that MdMIEL1 could mediate the ubiquitination and degradation of MdBBX7 by the 26S proteasome pathway. Genetic interaction analysis suggested that MdMIEL1 acts as an upstream factor of MdBBX7. In addition, MdMIEL1 was a negative regulator of the apple drought stress response. Taken together, our results illustrate the molecular mechanisms by which the MdMIEL1–MdBBX7 module influences the response of apple to drought stress.


2018 ◽  
Vol 102 ◽  
pp. 144-153 ◽  
Author(s):  
Xin-mei Zhang ◽  
Qiong Zhang ◽  
Chen-ling Pei ◽  
Xing Li ◽  
Xue-ling Huang ◽  
...  

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