The C. elegans Cell Death Specification Gene ces-1 Encodes a Snail Family Zinc Finger Protein

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.

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Worniu, a Snail family zinc-finger protein, is required for brain development inDrosophila

Developmental Dynamics ◽

10.1002/dvdy.20130 ◽

2004 ◽

Vol 231 (2) ◽

pp. 379-386 ◽

Cited By ~ 13

Author(s):

Shovon I. Ashraf ◽

Atish Ganguly ◽

John Roote ◽

Y. Tony Ip

Keyword(s):

Brain Development ◽

Zinc Finger ◽

Zinc Finger Protein ◽

Finger Protein ◽

Snail Family

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MCP-1 causes cardiomyoblast death via autophagy resulting from ER stress caused by oxidative stress generated by inducing a novel zinc-finger protein, MCPIP

Biochemical Journal ◽

10.1042/bj20090976 ◽

2010 ◽

Vol 426 (1) ◽

pp. 43-53 ◽

Cited By ~ 99

Author(s):

Craig W. Younce ◽

Pappachan E. Kolattukudy

Keyword(s):

Oxidative Stress ◽

Heart Failure ◽

Cell Death ◽

Er Stress ◽

Zinc Finger ◽

Zinc Finger Protein ◽

Beclin 1 ◽

Finger Protein ◽

Caspase 2 ◽

Specific Inhibitors

MCP-1 (monocyte chemotactic protein-1) plays a critical role in the development of heart failure that is known to involve apoptosis. How MCP-1 contributes to cell death involved in the development of heart disease is not understood. In the present study we show that MCP-1 causes death in cardiac myoblasts, H9c2 cells, by inducing oxidative stress which causes ER stress leading to autophagy via a novel zinc-finger protein, MCPIP (MCP-1-induced protein). MCPIP expression caused cell death, and knockdown of MCPIP attenuated MCP-1induced cell death. It caused induction of iNOS (inducible NO synthase), translocation of the NADPH oxidase subunit phox47 from the cytoplasm to the membrane, production of ROS (reactive oxygen species), and induction of ER (endoplasmic reticulum) stress markers HSP40 (heat-shock protein 40), PDI (protein disulfide-isomerase), GRP78 (guanine-nucleotide-releasing protein 78) and IRE1α (inositol-requiring enzyme 1α). It also caused autophagy, as indicated by beclin-1 induction, cleavage of LC3 (microtubule-associated protein 1 light chain 3) and autophagolysosome formation, and apoptosis, as indicated by caspase 3 activation and TUNEL (terminal deoxynucleotidyltransferase-mediated dUTP nick-end labelling) assay. Inhibitors of oxidative stress, including CeO2 nanoparticles, inhibited ROS formation, ER stress, autophagy and cell death. Specific inhibitors of ER stress inhibited autophagy and cell death as did knockdown of the ER stress signalling protein IRE1. Knockdown of beclin-1 and autophagy inhibitors prevented cell death. This cell death involved caspase 2 and caspase 12, as specific inhibitors of these caspases prevented MCPIP-induced cell death. Microarray analysis showed that MCPIP expression caused induction of a variety of genes known to be involved in cell death. MCPIP caused activation of JNK (c-Jun N-terminal kinase) and p38 and induction of p53 and PUMA (p53 up-regulated modulator of apoptosis). Taken together, these results suggest that MCPIP induces ROS/RNS (reactive nitrogen species) production that causes ER stress which leads to autophagy and apoptosis through caspase 2/12 and IRE1α–JNK/p38–p53–PUMA pathway. These results provide the first molecular insights into the mechanism by which elevated MCP-1 levels associated with chronic inflammation may contribute to the development of heart failure.

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The zinc finger protein ZAT11 modulates paraquat-induced programmed cell death in Arabidopsis thaliana

Acta Physiologiae Plantarum ◽

10.1007/s11738-013-1224-y ◽

2013 ◽

Vol 35 (6) ◽

pp. 1863-1871 ◽

Cited By ~ 16

Author(s):

Muhammad Kamran Qureshi ◽

Neerakkal Sujeeth ◽

Tsanko S. Gechev ◽

Jacques Hille

Keyword(s):

Arabidopsis Thaliana ◽

Cell Death ◽

Programmed Cell Death ◽

Zinc Finger ◽

Zinc Finger Protein ◽

Finger Protein

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TRA-1A regulates transcription of fog-3, which controls germ cell fate in C. elegans

Development ◽

10.1242/dev.127.14.3119 ◽

2000 ◽

Vol 127 (14) ◽

pp. 3119-3129 ◽

Cited By ~ 1

Author(s):

P. Chen ◽

R.E. Ellis

Keyword(s):

Transcriptional Regulation ◽

Sexual Identity ◽

Cell Fate ◽

Zinc Finger ◽

Germ Cells ◽

Zinc Finger Protein ◽

Rt Pcr ◽

C Elegans ◽

Finger Protein

In C. elegans, the zinc-finger protein TRA-1A is thought to be the final arbiter of somatic sexual identity. We show that fog-3, which is required for germ cells to become sperm rather than oocytes, is a target of TRA-1A. First, northern analyses and RT-PCR experiments indicate that expression of fog-3 is controlled by tra-1. Second, studies of double mutants show that this control could be direct. Third, the fog-3 promoter contains multiple sites that bind TRA-1A in gel shift assays, and mutations in these sites alter activity of fog-3 in vivo. These results establish fog-3 as one of the first known targets of transcriptional regulation by TRA-1A. Furthermore, they show that tra-1 controls a terminal regulator of sexual fate in germ cells, just as it is thought to do in the soma.

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