Evidence map›Paper›PMID 33990549›Full record

ArticleCell death & disease2021

CG6015 controls spermatogonia transit-amplifying divisions by epidermal growth factor receptor signaling in Drosophila testes.

Jun Yu, Qianwen Zheng, Zhiran Li, Yunhao Wu, Yangbo Fu, Xiaolong Wu, Dengfeng Lin, Cong Shen, Bo Zheng, Fei Sun

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
4.3field-weighted citation impact, top 5% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

12 citing papers in PubMed, 24 citations in OpenAlex.

  1. Article
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  4. Deficiency ofInternational journal of molecular sciences · 2024
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  10. Cells · 2023
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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

10 authors at 3 institutions in 1 country.

Jun Yu *Institute of Reproductive Medicine, School of Medicine, Nantong University, Nantong, China. yujun9117@126.com.ORCID http://orcid.org/0000-0003-3109-4102
Qianwen Zheng *Department of Gynecology, the Affiliated Hospital of Jiangsu University, Jiangsu University, Zhenjiang, China.
Zhiran Li *Institute of Reproductive Medicine, School of Medicine, Nantong University, Nantong, China.
Yunhao Wu *Institute of Reproductive Medicine, School of Medicine, Nantong University, Nantong, China.
Yangbo FuInstitute of Reproductive Medicine, School of Medicine, Nantong University, Nantong, China.
Xiaolong WuInstitute of Reproductive Medicine, School of Medicine, Nantong University, Nantong, China.
Dengfeng LinInstitute of Reproductive Medicine, School of Medicine, Nantong University, Nantong, China.
Cong ShenState Key Laboratory of Reproductive Medicine, Center for Reproduction and Genetics, Suzhou Municipal Hospital, The Affiliated Suzhou Hospital of Nanjing Medical University, Gusu School, Nanjing Medical University, Suzhou, China.
Bo ZhengState Key Laboratory of Reproductive Medicine, Center for Reproduction and Genetics, Suzhou Municipal Hospital, The Affiliated Suzhou Hospital of Nanjing Medical University, Gusu School, Nanjing Medical University, Suzhou, China. mansnoopy@163.com.ORCID http://orcid.org/0000-0002-1496-0753
Fei SunInstitute of Reproductive Medicine, School of Medicine, Nantong University, Nantong, China. sunfei@ntu.edu.cn.ORCID http://orcid.org/0000-0002-0870-8375
Nantong University · CNSuzhou Municipal Hospital · CNJiangsu University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Spermatogonia transit-amplifying (TA) divisions are crucial for the differentiation of germline stem cell daughters. However, the underlying mechanism is largely unknown. In the present study, we demonstrated that CG6015 was essential for spermatogonia TA-divisions and elongated spermatozoon development in Drosophila melanogaster. Spermatogonia deficient in CG6015 inhibited germline differentiation leading to the accumulation of undifferentiated cell populations. Transcriptome profiling using RNA sequencing indicated that CG6015 was involved in spermatogenesis, spermatid differentiation, and metabolic processes. Gene Set Enrichment Analysis (GSEA) revealed the relationship between CG6015 and the epidermal growth factor receptor (EGFR) signaling pathway. Unexpectedly, we discovered that phosphorylated extracellular regulated kinase (dpERK) signals were activated in germline stem cell (GSC)-like cells after reduction of CG6015 in spermatogonia. Moreover, Downstream of raf1 (Dsor1), a key downstream target of EGFR, mimicked the phenotype of CG6015, and germline dpERK signals were activated in spermatogonia of Dsor1 RNAi testes. Together, these findings revealed a potential regulatory mechanism of CG6015 via EGFR signaling during spermatogonia TA-divisions in Drosophila testes.

Indexed as

AnimalsCell DifferentiationDrosophilaDrosophila ProteinsErbB ReceptorsMaleReceptors, Invertebrate PeptideSpermatogoniaTestisDrosophila ProteinsEgfr protein, DrosophilaErbB ReceptorsReceptors, Invertebrate Peptide

Identifiers

PMID33990549
PMCPMC8121936
OpenAlexW3163218146

What Socratic holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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 Socratic graph.