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Updated: Dec 2, 2025
Cytological Analysis of Spermatogenesis: Live and Fixed Preparations of Drosophila Testes
Published on: January 20, 2014
Dlec1 is required for spermatogenesis and male fertility in mice
Yu Okitsu1, Mamoru Nagano1, Takahiro Yamagata2
1Department of Applied Life Sciences, Faculty of Agriculture, Shizuoka University, Shizuoka, Japan.
Abstract:
Deleted in lung and esophageal cancer 1 (DLEC1) is a tumour suppressor gene that is downregulated in various cancers in humans; however, the physiological and molecular functions of DLEC1 are still unclear. This study investigated the critical role of Dlec1 in spermatogenesis and male fertility in mice. Dlec1 was significantly expressed in testes, with dominant expression in germ cells. We disrupted Dlec1 in mice and analysed its function in spermatogenesis and male fertility. Dlec1 deletion caused male infertility due to impaired spermatogenesis. Spermatogenesis progressed normally to step 8 spermatids in Dlec1-/- mice, but in elongating spermatids, we observed head deformation, a shortened tail, and abnormal manchette organization. These phenotypes were similar to those of various intraflagellar transport (IFT)-associated gene-deficient sperm. In addition, DLEC1 interacted with tailless complex polypeptide 1 ring complex (TRiC) and Bardet-Biedl Syndrome (BBS) protein complex subunits, as well as α- and β-tubulin. DLEC1 expression also enhanced primary cilia formation and cilia length in A549 lung adenocarcinoma cells. These findings suggest that DLEC1 is a possible regulator of IFT and plays an essential role in sperm head and tail formation in mice.
Insights
Deleted in lung and esophageal cancer 1 (DLEC1) is crucial for male fertility. Its absence in mice impairs sperm development, leading to infertility and abnormal sperm structure, suggesting a role in intraflagellar transport.
Area of Science:
- Reproductive biology
- Molecular oncology
- Cell biology
Background:
- Deleted in lung and esophageal cancer 1 (DLEC1) is a tumor suppressor gene implicated in various human cancers.
- The precise physiological and molecular functions of DLEC1 remain largely uncharacterized.
- DLEC1 expression is notably reduced in several cancer types.
Purpose of the Study:
- To investigate the role of Dlec1 in spermatogenesis and male fertility in a mouse model.
- To elucidate the molecular mechanisms underlying Dlec1's function in germ cell development.
Main Methods:
- Generation of Dlec1-deficient mice (Dlec1-/-).
- Analysis of spermatogenesis progression and sperm morphology in Dlec1-/- mice.
- Biochemical assays to identify DLEC1 interacting proteins, including TRiC and BBS complex subunits.
- Assessment of primary cilia formation and length in lung cancer cells.
Main Results:
- Dlec1 is predominantly expressed in mouse testes, specifically in germ cells.
- Dlec1 deletion resulted in male infertility due to severe defects in spermatogenesis.
- Spermatids in Dlec1-/- mice exhibited head deformation, shortened tails, and abnormal manchette organization, resembling phenotypes of intraflagellar transport (IFT)-associated gene deficiencies.
- DLEC1 was found to interact with TRiC and BBS protein complex subunits, as well as tubulin.
- DLEC1 expression positively influenced primary cilia formation and length in A549 cells.
Conclusions:
- DLEC1 plays a critical role in spermatogenesis and male fertility in mice.
- The observed sperm defects suggest DLEC1's involvement in intraflagellar transport (IFT) pathways.
- DLEC1 is essential for proper sperm head and tail formation, potentially through its interactions with cytoskeletal and complex protein machinery.
