Targeted Deletion of Hsf1, 2, and 4 Genes in Mice

AbstractPhosphorus (P) deficiency is one of the major nutrient stresses restricting plant growth. The uptake of P by plants from soil is mainly mediated by the phosphate (Pi) transporters belonging to the PHT1 family. Multiple PHT1 genes from diverse plant species have been shown to be strongly up-regulated upon Pi starvation, however, the underlying mechanisms for the Pi-starvation-induced (PSI) up-regulation have not been well deciphered for most Pi transporter genes. Here, we reported a detailed dissection of the promoter activity of a PSI rice Pi transporter gene OsPT6, using the β-glucuronidase (GUS) reporter gene. OsPT6 promoter could drive GUS expression strongly in both roots and blades of rice plants grown under low P, but not high P. Cis-acting element analysis identified one copy of the P1BS motif and two copies of the W-box motif in OsPT6 promoter. Targeted deletion of the P1BS motif caused almost complete abolition of GUS induction in response to Pi starvation, irrespective of the presence or absence of the W-box motif, Four repeats of the P1BS motif fused to the CaMV35S minimal promoter was sufficient to induce GUS expression responsive to Pi starvation. Targeted deletion of the upstream W-box motif (W1) did not affect the GUS expression activity compared with the full-length OsPT6 promoter, while targeted deletion of the downstream W-box motif (W2) or both of the W-box motifs remarkably reduced the GUS induction rate upon Pi starvation. Our results proposed that the PSI response of OsPT6 was positively regulated by at least two elements, the sole P1BS and the downstream W-box, in its promoter, and the W-box-mediated up-regulation of OsPT6 might be highly dependent on the P1BS motif.

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An In Vivo Targeted Deletion of the Calmodulin-Binding Domain from Rice Glutamate Decarboxylase 3 (OsGAD3) Increases γ-Aminobutyric Acid Content in Grains

Rice ◽

10.1186/s12284-020-00380-w ◽

2020 ◽

Vol 13 (1) ◽

Author(s):

Kazuhito Akama ◽

Nadia Akter ◽

Hinako Endo ◽

Masako Kanesaki ◽

Masaki Endo ◽

...

Keyword(s):

Acid Content ◽

Glutamate Decarboxylase ◽

Binding Domain ◽

Aminobutyric Acid ◽

Targeted Deletion ◽

Calmodulin Binding

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Targeted deletion of HAI-1 increases prostasin proteolysis but decreases matriptase proteolysis in human keratinocytes

Human Cell ◽

10.1007/s13577-021-00488-1 ◽

2021 ◽

Author(s):

Dajun D. Lu ◽

Yayun Gu ◽

Sheng-Wen A. Li ◽

Robert J. Barndt ◽

Shih-Ming Huang ◽

...

Keyword(s):

Human Keratinocytes ◽

Targeted Deletion

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Targeted deletion of thearaoperon ofSalmonella typhimuriumenhances L-arabinose accumulation and drives PBAD-promoted expression of anti-cancer toxins and imaging agents

Cell Cycle ◽

10.4161/15384101.2014.949527 ◽

2014 ◽

Vol 13 (19) ◽

pp. 3112-3120 ◽

Cited By ~ 10

Author(s):

Hyun Hong ◽

Daejin Lim ◽

Geun-Joong Kim ◽

Seung-Hwan Park ◽

Hyeon Sik Kim ◽

...

Keyword(s):

Imaging Agents ◽

Targeted Deletion ◽

Anti Cancer

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MFng Is Dispensable for Mouse Pancreas Development and Function

Molecular and Cellular Biology ◽

10.1128/mcb.01644-08 ◽

2009 ◽

Vol 29 (8) ◽

pp. 2129-2138 ◽

Cited By ~ 18

Author(s):

Per Svensson ◽

Ingela Bergqvist ◽

Stefan Norlin ◽

Helena Edlund

Keyword(s):

Cell Differentiation ◽

Notch Signaling ◽

Pancreas Development ◽

Loss Of Function ◽

Pancreatic Cell ◽

Targeted Deletion ◽

Mouse Pancreas ◽

Pancreatic Progenitor ◽

Pancreatic Progenitor Cells ◽

And Function

ABSTRACT Notch signaling regulates pancreatic cell differentiation, and mutations of various Notch signaling components result in perturbed pancreas development. Members of the Fringe family of β1,3-N-acetylglucosaminyltransferases, Manic Fringe (MFng), Lunatic Fringe (LFng), and Radical Fringe (RFng), modulate Notch signaling, and MFng has been suggested to regulate pancreatic endocrine cell differentiation. We have characterized the expression of the three mouse Fringe genes in the developing mouse pancreas between embryonic days 9 and 14 and show that the expression of MFng colocalized with the proendocrine transcription factor Ngn3. In contrast, the expression of LFng colocalized with the exocrine marker Ptf1a, whereas RFng was not expressed. Moreover, we show that expression of MFng is lost in Ngn3 mutant mice, providing evidence that MFng is genetically downstream of Ngn3. Gain- and loss-of-function analyses of MFng by the generation of mice that overexpress MFng in early pancreatic progenitor cells and mice with a targeted deletion of MFng provide, however, evidence that MFng is dispensable for pancreas development and function, since no pancreatic defects in these mice were observed.

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