The Sertoli-Germ Cell Communication Network in Mammals

Jégou, Bernard

doi:10.1016/s0074-7696(08)60766-4

Cited by 304 publications

(193 citation statements)

References 406 publications

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“…5,11,19 We next asked whether the disorganized cytoskeleton structures in testis were directly or indirectly caused by autophagy disruption. To test this, primary AMHatg5 ¡/¡ and control Sertoli cells were isolated, and the cytoskeleton structures were detected in vitro by immunofluorescence of phalloidin.…”

Section: Disordered Tubulobulbar-complex Distribution In the Autophagmentioning

confidence: 99%

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Autophagy is required for ectoplasmic specialization assembly in sertoli cells

et al. 2016

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The ectoplasmic specialization (ES) is essential for Sertoli-germ cell communication to support all phases of germ cell development and maturity. Its formation and remodeling requires rapid reorganization of the cytoskeleton. However, the molecular mechanism underlying the regulation of ES assembly is still largely unknown. Here, we show that Sertoli cell-specific disruption of autophagy influenced male mouse fertility due to the resulting disorganized seminiferous tubules and spermatozoa with malformed heads. In autophagy-deficient mouse testes, cytoskeleton structures were disordered and ES assembly was disrupted. The disorganization of the cytoskeleton structures might be caused by the accumulation of a negative cytoskeleton organization regulator, PDLIM1, and these defects could be partially rescued by Pdlim1 knockdown in autophagy-deficient Sertoli cells. Altogether, our works reveal that the degradation of PDLIM1 by autophagy in Sertoli cells is important for the proper assembly of the ES, and these findings define a novel role for autophagy in Sertoli cell-germ cell communication.

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Section: Disordered Tubulobulbar-complex Distribution In the Autophagmentioning

confidence: 99%

“…3,4 At all stages of spermatogenesis, Sertoli cells and germ cells have developed a set of communication devices that are involved in attachment, displacement, degeneration, and cellcell transfer of signaling molecules and cellular materials. 5 This Sertoli-germ cell communication is necessary for successful spermatogenesis.…”

Section: Introductionmentioning

confidence: 99%

Autophagy is required for ectoplasmic specialization assembly in sertoli cells

et al. 2016

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“…Within the seminiferous epithelium, communication and contact is mainly mediated by the somatic SC (Byers et al 1993, Enders 1993, Jégou 1993, Russel 1993, Sharpe 1993, Risley et al 2002. For this purpose, mature SC form a complex network of specific intercellular junctions with individual adjacent GC populations and each other.…”

Section: Sc Btb and Junctional Proteinsmentioning

confidence: 99%

Blood–testis barrier and Sertoli cell function: lessons from SCCx43KO mice

Gerber¹,

Heinrich²,

Brehm³

2016

Reproduction

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The gap junction protein connexin43 (CX43) plays a vital role in mammalian spermatogenesis by allowing for direct cytoplasmic communication between neighbouring testicular cells. In addition, different publications suggest that CX43 in Sertoli cells (SC) might be important for blood-testis barrier (BTB) formation and BTB homeostasis. Thus, through the use of the Cre-LoxP recombination system, a transgenic mouse line was developed in which only SC are deficient of the gap junction protein, alpha 1 (Gja1) gene. Gja1 codes for the protein CX43. This transgenic mouse line has been commonly defined as the SC specific CX43 knockout (SCCx43KO) mouse line. Within the seminiferous tubule, SC aid in spermatogenesis by nurturing germ cells and help them to proliferate and mature. Owing to the absence of CX43 within the SC, homozygous KO mice are infertile, have reduced testis size, and mainly exhibit spermatogenesis arrest at the level of spermatogonia, seminiferous tubules containing only SC (SC-only syndrome) and intratubular SC-clusters. Although the SC specific KO of CX43 does not seem to have an adverse effect on BTB integrity, CX43 influences BTB composition as the expression pattern of different BTB proteins (like OCCLUDIN, b-CATENIN, N-CADHERIN, and CLAUDIN11) is altered in mutant males. The supposed roles of CX43 in dynamic BTB regulation, BTB assembly and/or disassembly and its possible interaction with other junctional proteins composing this unique barrier are discussed. Data collectively indicate that CX43 might represent an important regulator of dynamic BTB formation, composition and function.Reproduction (2016) 151 R15-R27

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“…These observations raise the question whether Sertoli cells and germ cells are independently affected by the lack of RXRf~ or whether one cell type is primarily affected. Abnormal Sertoli cells could be impaired in their ability to correctly assist the maturation and release of spermatids (Redenbach and Vogel 1991;Jegou 1993;Griswold 1995); alternatively, the lipid accumulation in Sertoli cells could result from widespread phagocytosis of abnormal spermatids (Russell et al 1990).…”

Section: Abnormal Spermatogenesis and Degeneration Of The Seminiferoumentioning

confidence: 99%

“…It is well established that Sertoli cell/germ cell interactions are critical for sperm maturation and spermiation (for review, see Jegou 1993;Griswold 1995). Each maturing spermatid is encased by Sertoli cell cytoplasm that is thought to assist its maturation and its release by as yet poorly understood mechanisms.…”

Section: Abnormal Spermatogenesis and Degeneration Of The Seminiferoumentioning

confidence: 99%

Abnormal spermatogenesis in RXR beta mutant mice.

Kastner¹,

Mark²,

Leid³

et al. 1996

Genes Dev.

303

214

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We have generated mouse lines in which the RXRI3 gene was disrupted by homologous recombination. Approximately 50% of the RXR~ homozygous mutants died before or at birth, but those that survived appeared normal except that the males were sterile, owing to oligo-astheno-teratozoospermia. Failure of spermatid release occurred within the germinal epithelium, and the epididymis contained very few spermatozoa that, in addition, exhibited abnormal acrosomes and tails. There was a progressive accumulation of lipids within the mutant Sertoli cells, which were histochemically characterized as unsaturated triglycerides. In old mutant males, progressive degeneration of the germinal epithelium occurred, ending with the formation of acellular lipid-filled tubules. The selective expression of RXR[~ in Sertoli cells, together with the timing of appearence of the histological abnormalities, suggests that the primary defect resulting from the mutation resides in these cells.

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The Sertoli-Germ Cell Communication Network in Mammals

Cited by 304 publications

References 406 publications

Autophagy is required for ectoplasmic specialization assembly in sertoli cells

Autophagy is required for ectoplasmic specialization assembly in sertoli cells

Blood–testis barrier and Sertoli cell function: lessons from SCCx43KO mice

Abnormal spermatogenesis in RXR beta mutant mice.

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