Faculty Opinions recommendation of Two distinct types of neuronal asymmetries are controlled by the Caenorhabditis elegans zinc finger transcription factor die-1.

The mutation lin-26(n156) prevents vulva formation in C. elegans by transforming the vulval precursor cells into neurons or neuroblasts. We have isolated and characterized three new lin-26 alleles, which result in embryonic lethality. These mutations cause a few other hypodermal cells to express a neural fate and most hypodermal cells to degenerate. lin-26 encodes a presumptive zinc-finger transcription factor. Our data indicate that lin-26 is required for cells to acquire the hypodermal fate.

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Two distinct types of neuronal asymmetries are controlled by the Caenorhabditis elegans zinc finger transcription factor die-1

Genes & Development ◽

10.1101/gad.233643.113 ◽

2013 ◽

Vol 28 (1) ◽

pp. 34-43 ◽

Cited By ~ 20

Author(s):

L. Cochella ◽

B. Tursun ◽

Y.-W. Hsieh ◽

S. Galindo ◽

R. J. Johnston ◽

...

Keyword(s):

Transcription Factor ◽

Caenorhabditis Elegans ◽

Zinc Finger ◽

Zinc Finger Transcription Factor

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A Left/Right Asymmetric Neuronal Differentiation Program Is Controlled by the Caenorhabditis elegans LSY-27 Zinc-Finger Transcription Factor

Genetics ◽

10.1534/genetics.111.129064 ◽

2011 ◽

Vol 188 (3) ◽

pp. 753-759 ◽

Cited By ~ 8

Author(s):

Feifan Zhang ◽

M. Maggie O'Meara ◽

Oliver Hobert

Keyword(s):

Transcription Factor ◽

Caenorhabditis Elegans ◽

Neuronal Differentiation ◽

Zinc Finger ◽

Zinc Finger Transcription Factor

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Faculty Opinions recommendation of The zinc finger transcription factor Th-POK regulates CD4 versus CD8 T-cell lineage commitment.

Faculty Opinions – Post-Publication Peer Review of the Biomedical Literature ◽

10.3410/f.1024248.290751 ◽

2005 ◽

Author(s):

Kyoko Hayakawa

Keyword(s):

Transcription Factor ◽

T Cell ◽

Zinc Finger ◽

Cell Lineage ◽

Cd8 T Cell ◽

Lineage Commitment ◽

Zinc Finger Transcription Factor

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Faculty Opinions recommendation of Regulation of Aluminum Resistance in Arabidopsis Involves the SUMOylation of the Zinc Finger Transcription Factor STOP1.

Faculty Opinions – Post-Publication Peer Review of the Biomedical Literature ◽

10.3410/f.738884406.793579957 ◽

2020 ◽

Author(s):

Ramón Serrano

Keyword(s):

Transcription Factor ◽

Zinc Finger ◽

Zinc Finger Transcription Factor ◽

Aluminum Resistance

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The apple C2H2-type zinc finger transcription factor MdZAT10 positively regulates JA-induced leaf senescence by interacting with MdBT2

Horticulture Research ◽

10.1038/s41438-021-00593-0 ◽

2021 ◽

Vol 8 (1) ◽

Author(s):

Kuo Yang ◽

Jian-Ping An ◽

Chong-Yang Li ◽

Xue-Na Shen ◽

Ya-Jing Liu ◽

...

Keyword(s):

Mass Spectrometry ◽

Transcription Factor ◽

Liquid Chromatography ◽

Zinc Finger ◽

Leaf Senescence ◽

Transcriptional Activity ◽

Molecular Mechanisms ◽

Liquid Chromatography Mass Spectrometry ◽

Zinc Finger Transcription Factor ◽

Insight Into

AbstractJasmonic acid (JA) plays an important role in regulating leaf senescence. However, the molecular mechanisms of leaf senescence in apple (Malus domestica) remain elusive. In this study, we found that MdZAT10, a C2H2-type zinc finger transcription factor (TF) in apple, markedly accelerates leaf senescence and increases the expression of senescence-related genes. To explore how MdZAT10 promotes leaf senescence, we carried out liquid chromatography/mass spectrometry screening. We found that MdABI5 physically interacts with MdZAT10. MdABI5, an important positive regulator of leaf senescence, significantly accelerated leaf senescence in apple. MdZAT10 was found to enhance the transcriptional activity of MdABI5 for MdNYC1 and MdNYE1, thus accelerating leaf senescence. In addition, we found that MdZAT10 expression was induced by methyl jasmonate (MeJA), which accelerated JA-induced leaf senescence. We also found that the JA-responsive protein MdBT2 directly interacts with MdZAT10 and reduces its protein stability through ubiquitination and degradation, thereby delaying MdZAT10-mediated leaf senescence. Taken together, our results provide new insight into the mechanisms by which MdZAT10 positively regulates JA-induced leaf senescence in apple.

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Specific collagens maintain the cuticle permeability barrier in Caenorhabditis elegans

Genetics ◽

10.1093/genetics/iyaa047 ◽

2021 ◽

Author(s):

Anjali Sandhu ◽

Divakar Badal ◽

Riya Sheokand ◽

Shalini Tyagi ◽

Varsha Singh

Keyword(s):

Transcription Factor ◽

Caenorhabditis Elegans ◽

Barrier Function ◽

Permeability Barrier ◽

Nematode Caenorhabditis Elegans ◽

Zinc Finger Transcription Factor ◽

Outermost Layer ◽

C Elegans ◽

Receptor Mutant ◽

Antioxidant Machinery

Abstract Collagen enriched cuticle forms the outermost layer of skin in nematode Caenorhabditis elegans. The nematode’s genome encodes 177 collagens, but little is known about their role in maintaining the structure or barrier function of the cuticle. In this study, we found six permeability determining (PD) collagens. Loss of any of these PD collagens- DPY-2, DPY-3, DPY-7, DPY-8, DPY-9, and DPY-10- led to enhanced susceptibility of nematodes to paraquat (PQ) and antihelminthic drugs levamisole and ivermectin. Upon exposure to paraquat, PD collagen mutants accumulated more PQ and incurred more damage and death despite the robust activation of antioxidant machinery. We find that BLMP-1, a zinc finger transcription factor, maintains the barrier function of the cuticle by regulating the expression of PD collagens. We show that the permeability barrier maintained by PD collagens acts in parallel to FOXO transcription factor DAF-16 to enhance survival of insulin-like receptor mutant, daf-2. In all, this study shows that PD collagens regulate cuticle permeability by maintaining the structure of C. elegans cuticle and thus provide protection against exogenous toxins.

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