Evidence map›Paper›PMID 39305158›Full record

ArticleDevelopment, growth & differentiation2024

Establishment and characterization of mouse lines useful for endogenous protein degradation via an improved auxin-inducible degron system (AID2).

Hatsune Makino-Itou, Noriko Yamatani, Akemi Okubo, Makoto Kiso, Rieko Ajima, Masato T Kanemaki, Yumiko Saga

Abstract read
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Article in Development, growth & differentiation, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

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3 · Its place in the literature

Who cites it

7 citing papers in PubMed.

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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors.

Hatsune Makino-ItouDepartment of Gene Function and Phenomics, National Institute of Genetics, Research Organization of Information and Systems (ROIS), Mishima, Japan.
Noriko YamataniDivision for Development of Genetic-Engineered Mouse Resource, National Institute of Genetics, Mishima, Japan.
Akemi OkuboDepartment of Gene Function and Phenomics, National Institute of Genetics, Research Organization of Information and Systems (ROIS), Mishima, Japan.
Makoto KisoDivision for Development of Genetic-Engineered Mouse Resource, National Institute of Genetics, Mishima, Japan.
Rieko AjimaDepartment of Gene Function and Phenomics, National Institute of Genetics, Research Organization of Information and Systems (ROIS), Mishima, Japan.
Masato T KanemakiDepartment of Genetics, Graduate Institute for Advanced Studies, Mishima, Japan.
Yumiko SagaDepartment of Gene Function and Phenomics, National Institute of Genetics, Research Organization of Information and Systems (ROIS), Mishima, Japan.ORCID https://orcid.org/0000-0001-9198-5164

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The development of new technologies opens new avenues in the research field. Gene knockout is a key method for analyzing gene function in mice. Currently, conditional gene knockout strategies are employed to examine temporal and spatial gene function. However, phenotypes are sometimes not observed because of the time required for depletion due to the long half-life of the target proteins. Protein knockdown using an improved auxin-inducible degron system, AID2, overcomes such difficulties owing to rapid and efficient target depletion. We observed depletion of AID-tagged proteins within a few to several hours by a simple intraperitoneal injection of the auxin analog, 5-Ph-IAA, which is much shorter than the time required for target depletion using conditional gene knockout. Importantly, the loss of protein is reversible, making protein knockdown useful to measure the effects of transient loss of protein function. Here, we also established several mouse lines useful for AID2-medicated protein knockdown, which include knock-in mouse lines in the ROSA26 locus; one expresses TIR1(F74G), and the other is the reporter expressing AID-mCherry. We also established a germ-cell-specific TIR1 line and confirmed the protein knockdown specificity. In addition, we introduced an AID tag to an endogenous protein, DCP2 via the CAS9-mediated gene editing method. We confirmed that the protein was effectively eliminated by TIR1(F74G), which resulted in the similar phenotype observed in knockout mouse within 20 h.

Indexed as

Indoleacetic AcidsAnimalsDegronsGene Knockdown TechniquesMiceProteolysisIndoleacetic AcidsCas9 gene editingdegronknock‐in mouseprotein knockdownROSA26 locustransgenic mouse

Identifiers

PMID39305158
PMCPMC11482630

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.