Flotillin-2 is an acrosome-related protein involved in mouse spermiogenesis

Wu, Yibo; Chen, Xin; Wang, Shuai; Jiang, Min; Zheng, Bo; Zhou, Quan; Bi, Ye; Zhou, Zuomin; Huang, Xiaoyan; Sha, Jiahao

doi:10.7555/jbr.26.20120030

Cited by 11 publications

(5 citation statements)

References 36 publications

(49 reference statements)

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“…For example, flotillins, members of a ubiquitous family of membrane proteins, are involved in numerous cellular processes and are also essential for spermatozoon functionality. In spermatozoa, the acrosome is a cap-like structure that enables fusion with the egg, and proteins from the flotillin family have been shown to be involved in its biogenesis and functionality (52). In our study, flotillin-1 (I.D.…”

Section: Discussionmentioning

confidence: 77%

Proteogenomics of Gammarus fossarum to Document the Reproductive System of Amphipods

Trapp

Geffard²,

Imbert

et al. 2014

Molecular & Cellular Proteomics

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Because of their ecological importance, amphipod crustacea are employed worldwide as test species in environmental risk assessment. Although proteomics allows new insights into the molecular mechanisms related to the stress response, such investigations are rare for these organisms because of the lack of comprehensive protein sequence databases. Here, we propose a proteogenomic approach for identifying specific proteins of the freshwater amphipod Gammarus fossarum, a keystone species in European freshwater ecosystems. After deep RNA sequencing, we created a comprehensive ORF database. Next-generation proteomics, relying on ultra-rapid and subparts-per-million mass spectrometry analyzers, is able to offer in-depth insights into the molecular players sustaining the physiology of complex organisms. Identifying and quantitating thousands of proteins has become, over the past decade, a routine task for most proteomic platforms with the development of high-throughput shotgun proteomics. The interpretation of large-scale MS/MS data is only possible if a highquality database of nucleic acid sequences is available. Homology-driven proteomics using cross-species matching is a first alternative if the genome of interest is unknown, and de novo sequencing (i.e. interpretation of MS/MS data to establish the exact sequence of each peptide from scratch) is another possibility. However, major drawbacks of these two approaches lead to a scarcity of results as soon as a non-model organism, distantly related to a sequenced organism, is analyzed. Indeed, only highly conserved and ubiquitous proteins will be identified and carefully annotated with such approaches.

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Section: Discussionmentioning

confidence: 77%

Proteogenomics of Gammarus fossarum to Document the Reproductive System of Amphipods

Trapp

Geffard²,

Imbert

et al. 2014

Molecular & Cellular Proteomics

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“…Using knockout mouse (−/−) models, a number of genes (e.g., Dpy19l2 , 18 Pick1 , 19 Dnah1 , 20 Gopc , 21 Vps54 , 22 Hrb , 23 Zpbp1 , 24 Ck2α′ , 25 Hsp90b1 , 26 Gba2 , 27 Spaca1 , 28 Atg7 , 29 Smap2 , 30 Fads2 , 31 Flotillin-2 , 32 Ccdc136 , 33 Pcsk4 34 and Hiat1 35 ) have been found to trigger globozoospermia. Among them, deletions and/or mutations in SPATA16 , 36, 37 PICK1 , 38 DPY19L2 , 39 ZPBP1 40 and DNAH1 41 have been identified in globozoospermia patients.…”

Section: Globozoospermia-related Proteins: Roles In Acrosomementioning

confidence: 99%

The control of male fertility by spermatid-specific factors: searching for contraceptive targets from spermatozoon’s head to tail

et al. 2016

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Male infertility due to abnormal spermatozoa has been reported in both animals and humans, but its pathogenic causes, including genetic abnormalities, remain largely unknown. On the other hand, contraceptive options for men are limited, and a specific, reversible and safe method of male contraception has been a long-standing quest in medicine. Some progress has recently been made in exploring the effects of spermatid-specifical genetic factors in controlling male fertility. A comprehensive search of PubMed for articles and reviews published in English before July 2016 was carried out using the search terms ‘spermiogenesis failure', ‘globozoospermia', ‘spermatid-specific', ‘acrosome', ‘infertile', ‘manchette', ‘sperm connecting piece', ‘sperm annulus', ‘sperm ADAMs', ‘flagellar abnormalities', ‘sperm motility loss', ‘sperm ion exchanger' and ‘contraceptive targets'. Importantly, we have opted to focus on articles regarding spermatid-specific factors. Genetic studies to define the structure and physiology of sperm have shown that spermatozoa appear to be one of the most promising contraceptive targets. Here we summarize how these spermatid-specific factors regulate spermiogenesis and categorize them according to their localization and function from spermatid head to tail (e.g., acrosome, manchette, head-tail conjunction, annulus, principal piece of tail). In addition, we emphatically introduce small-molecule contraceptives, such as BRDT and PPP3CC/PPP3R2, which are currently being developed to target spermatogenic-specific proteins. We suggest that blocking the differentiation of haploid germ cells, which rarely affects early spermatogenic cell types and the testicular microenvironment, is a better choice than spermatogenic-specific proteins. The studies described here provide valuable information regarding the genetic and molecular defects causing male mouse infertility to improve our understanding of the importance of spermatid-specific factors in controlling fertility. Although a male contraceptive ‘pill' is still many years away, research into the production of new small-molecule contraceptives targeting spermatid-specific proteins is the right avenue.

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“…In mice, round spermatids begin to appear at approximately 3 weeks of age; transcription and translation mostly cease during this process, and siRNAs introduced into the seminiferous tubule at this time point would degrade the targeting mRNA, which could not be replaced by newly transcribed mRNA [34]. Thus, the protein level of the targeting gene will be reduced for a relatively long period.…”

Section: Discussionmentioning

confidence: 99%

Decreased Expression of KIFC1 in Human Testes with Globozoospermic Defects

Zhi

Chen

et al. 2016

Genes

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Globozoospermia is a rare (prevalence of <0.1%) but severe male infertility condition. In our previous study, we found that robust KIFC1 immunostaining was detected in the human elongating/elongated spermatids during human acrosomogenesis. However, the relationship between the decreased expression of KIFC1 and human globozoospermia remains largely unknown. Testicular biopsies of 30 globozoospermia and 30 obstructive azoospermia patients who underwent infertility evaluation and treatment were utilized in this study. Reverse transcriptase polymerase chain reaction (RT-PCR), Western blots, immunohistochemistry, an in vivo model, and intratesticular injection of small inhibitory RNA (siRNA) against the Kifc1 gene were employed, and sperm abnormalities were evaluated by hematoxylin and eosin (H&E) staining and immunocytochemistry. We revealed that the testicular level of KIFC1 mRNA in globozoospermia was significantly reduced compared with that in obstructive azoospermia, and the KIFC1 protein was barely detectable in testicular specimens in 30% (9 of 30) of patients with globozoospermia. Furthermore, knockdown of the Kifc1 gene in mice increased the percentage of sperm with globozoospermic defects (26.5%). Decreased KIFC1 expression was mainly observed in the testes of patients with globozoospermia at the spermatid stage, which may be useful for counseling and management of such patients.

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Flotillin-2 is an acrosome-related protein involved in mouse spermiogenesis

Cited by 11 publications

References 36 publications

Proteogenomics of Gammarus fossarum to Document the Reproductive System of Amphipods

Proteogenomics of Gammarus fossarum to Document the Reproductive System of Amphipods

The control of male fertility by spermatid-specific factors: searching for contraceptive targets from spermatozoon’s head to tail

Decreased Expression of KIFC1 in Human Testes with Globozoospermic Defects

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