Microtubules and spermatogenesis

O’Donnell, Liza; O'Bryan, Moira K

doi:10.1016/j.semcdb.2014.01.003

Cited by 175 publications

(152 citation statements)

References 97 publications

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“…1 MTs, on the other hand, are polarized cytoskeletal elements that lie adjacent to the F-actin network and serve as tracks to assist in the transport of endocytic vesicles, organelles, and germ cells, in particular preleptotene spermatocytes or spermatids across the BTB or apical compartment, respectively, during the epithelial cycle. 2,3 Our data suggest that AKAP9 regulation of MTs may be essential for these functions. End-binding proteins (þTIPs), such as EB1, interact with the plus ends of growing MTs, capture MTs at cortical sites to establish an asymmetric MT network, and regulate MT linkage to actin.…”

Section: Discussionmentioning

confidence: 75%

“…1 However, little is known about the role and regulation of the microtubule (MT) network in BTB dynamics and spermatogenesis. 2,3 Signal-organizing scaffolding proteins, called AKAPs, compartmentalize and ensure specificity of cAMP-signaling networks. 4 AKAPs localize to discrete cell compartments and bind protein kinase A (PKA) and in some cases the cAMP-responsive guanine exchange factor Epac1 to spatially restrict the activity of these proteins toward a subset of effector molecules.…”

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confidence: 99%

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AKAP9, a Regulator of Microtubule Dynamics, Contributes to Blood-Testis Barrier Function

Venkatesh

Mruk

Herter

et al. 2016

The American Journal of Pathology

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The blood-testis barrier (BTB), formed between adjacent Sertoli cells, undergoes extensive remodeling to facilitate the transport of preleptotene spermatocytes across the barrier from the basal to apical compartments of the seminiferous tubules for further development and maturation into spermatozoa. The actin cytoskeleton serves unique structural and supporting roles in this process, but little is known about the role of microtubules and their regulators during BTB restructuring. The large isoform of the cAMP-responsive scaffold protein AKAP9 regulates microtubule dynamics and nucleation at the Golgi. We found that conditional deletion of Akap9 in mice after the initial formation of the BTB at puberty leads to infertility. Akap9 deletion results in marked alterations in the organization of microtubules in Sertoli cells and a loss of barrier integrity despite a relatively intact, albeit more apically localized F-actin and BTB tight junctional proteins. These changes are accompanied by a loss of haploid spermatids due to impeded meiosis. The barrier, however, progressively reseals in older Akap9 null mice, which correlates with a reduction in germ cell apoptosis and a greater incidence of meiosis. However, spermiogenesis remains defective, suggesting additional roles for AKAP9 in this process. Together, our data suggest that AKAP9 and, by inference, the regulation of the microtubule network are critical for BTB function and subsequent germ cell development during spermatogenesis. (Am J Pathol 2016, 186: 270e284; http://dx

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Section: Discussionmentioning

confidence: 75%

mentioning

confidence: 99%

AKAP9, a Regulator of Microtubule Dynamics, Contributes to Blood-Testis Barrier Function

Venkatesh

Mruk

Herter

et al. 2016

The American Journal of Pathology

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“…3A), which was consistent with previous descriptions. 40 However, in the AMHatg5 ¡/¡ testes, both the linear structure along the axis and the cage-like structure around the nucleus were abolished (Fig. 3A).…”

Section: The Apical Es Is Disrupted In Sertoli Cell-specific Autophagmentioning

confidence: 95%

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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“…3,23,24,26,27 In terms of reproductive toxicant administration, abnormal acrosome development during early spermiogenesis could suggest an action on the round spermatid Golgi apparatus, vesicle-mediated trafficking, 23 F-actin and myosin-mediated vesicle trafficking 28 or microtubule dynamics. 29 Detachment of acrosomes later in spermatid elongation could reflect an action on the perinuclear theca. 24 …”

Section: Abnormal Acrosome Developmentmentioning

confidence: 99%

Mechanisms of spermiogenesis and spermiation and how they are disturbed

2014

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Haploid round spermatids undergo a remarkable transformation during spermiogenesis. The nucleus polarizes to one side of the cell as the nucleus condenses and elongates, and the microtubule-based manchette sculpts the nucleus into its species-specific head shape. The assembly of the central component of the sperm flagellum, known as the axoneme, begins early in spermiogenesis, and is followed by the assembly of secondary structures needed for normal flagella. The final remodelling of the mature elongated spermatid occurs during spermiation, when the spermatids line up along the luminal edge, shed their residual cytoplasm and are ultimately released into the lumen. Defects in spermiogenesis and spermiation are manifested as low sperm number, abnormal sperm morphology and poor motility and are commonly observed during reproductive toxicant administration, as well as in genetically modified mouse models of male infertility. This chapter summarizes the major physiological processes and the most commonly observed defects in spermiogenesis and spermiation, to aid in the diagnosis of the potential mechanisms that could be perturbed by experimental manipulation such as reproductive toxicant administration. Signature LesionThere are a number of signature lesions that could indicate a disturbance in spermiogenesis or spermiation. These would include misshapen heads and/or tails of elongating/elongated spermatids. Multinucleated round spermatids may reflect disturbances in spermiogenesis, but could also reflect altered Sertoli cell function. Disruption of spermiation could present itself as spermatid retention at the lumen of post stage VIII tubules, failure of elongated spermatids to ascend to the lumen of stage VII/ VIII tubules, or phagocytosis of mature spermatids at the base of tubules in stages VII through to approximately XII (in mice) or XIV (in rats). The changes might occur in isolation or in combination with one another.

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Microtubules and spermatogenesis

Cited by 175 publications

References 97 publications

AKAP9, a Regulator of Microtubule Dynamics, Contributes to Blood-Testis Barrier Function

AKAP9, a Regulator of Microtubule Dynamics, Contributes to Blood-Testis Barrier Function

Autophagy is required for ectoplasmic specialization assembly in sertoli cells

Mechanisms of spermiogenesis and spermiation and how they are disturbed

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