Inactivation of Dicer1 has a severe cumulative impact on the formation of mature germ cells in mouse testes

Liu, Dekang; Li, Liangyun; Fu, Heling; Li, Shuzhen; Li, Jianmin

doi:10.1016/j.bbrc.2012.04.118

Cited by 28 publications

(22 citation statements)

References 33 publications

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“…Mounting evidence indicates small non-coding RNAs, such as microRNAs RESEARCH ARTICLE miRNAs in male germline stem cells (miRNAs), play essential roles in maintenance of stem and progenitor cell populations by regulating the stability and translation of mRNAs (Ghildiyal and Zamore, 2009). Importantly, recent studies with mice showed that miRNA biogenesis in germ cells is required for normal spermatogenesis (Maatouk et al, 2008;Korhonen et al, 2011;Romero et al, 2011;Liu et al, 2012). However, the role of individual miRNAs for maintenance of specific stages of germ cell development is largely unexplored.…”

Section: Introductionmentioning

confidence: 99%

MicroRNAs 221 and 222 regulate the undifferentiated state in mammalian male germ cells

et al. 2013

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SUMMARYContinuity of cycling cell lineages relies on the activities of undifferentiated stem cell-containing subpopulations. Transition to a differentiating state must occur periodically in a fraction of the population to supply mature cells, coincident with maintenance of the undifferentiated state in others to sustain a foundational stem cell pool. At present, molecular mechanisms regulating these activities are poorly defined for most cell lineages. Spermatogenesis is a model process that is supported by an undifferentiated spermatogonial population and transition to a differentiating state involves attained expression of the KIT receptor. We found that impaired function of the X chromosome-clustered microRNAs 221 and 222 (miR-221/222) in mouse undifferentiated spermatogonia induces transition from a KIT -to a KIT + state and loss of stem cell capacity to regenerate spermatogenesis. Both Kit mRNA and KIT protein abundance are influenced by miR-221/222 function in spermatogonia. Growth factors that promote maintenance of undifferentiated spermatogonia upregulate miR-221/222 expression; whereas exposure to retinoic acid, an inducer of spermatogonial differentiation, downregulates miR-221/222 abundance. Furthermore, undifferentiated spermatogonia overexpressing miR-221/222 are resistant to retinoic acid-induced transition to a KIT + state and are incapable of differentiation in vivo. These findings indicate that miR-221/222 plays a crucial role in maintaining the undifferentiated state of mammalian spermatogonia through repression of KIT expression.

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Section: Introductionmentioning

confidence: 99%

MicroRNAs 221 and 222 regulate the undifferentiated state in mammalian male germ cells

et al. 2013

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“…Удаление Dicer1 в линии мышиных мужских поло-вых клеток непосредственно перед рождением с по-мощью Ddx4 промотеруправляемой Cre-рекомбиназы привело к возникновению серьезных дефектов в мейо-тических и постмейотических половых клетках [78,95]. Произошла задержка в прохождении профазы I мейо-за во время сперматогенеза, значительно увеличилось количество апоптотических сперматоцитов, что, в свою очередь, привело к уменьшению числа сперматид.…”

Section: микрорнк в мейотических и постмейотических клеткахunclassified

“…Подобные дефекты возникли и у мо-дельных мышей с нокаутом Ddx4-Cre-Dicer1: морфо-логия сперматозоидов в эпидидимисе была атипич-ной -с маленькими деформированными головками и атипичной структурой жгутиков, кроме того, значи-тельно снизилось количество продуцируемых сперма-тозоидов. Удаление Dicer1 в ранних сперматогониях с помощью модели Stra8-Cre привело к серьезным на-рушениям в гаплоидной дифференцировке [97,98] [95,96]. Они имели атипичную форму го-ловки сперматозоидов и неправильную компактиза-цию хроматина [99].…”

Section: микрорнк в мейотических и постмейотических клеткахunclassified

Role of microRNAs in spermatogenesis

Руднева¹,

Хаченкова²

2016

Androl. genit. hir.

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“…While mutant embryos generated from Dicer1-null oocytes failed to proceed to a twocell embryo, mice homozygous for a hypomorphic allele developed normally except for female infertility associated with corpus luteum insufficiency . Furthermore, mice with Dicer1 deleted specifically in germ cells showed arrest of spermatogenesis Liu et al, 2012).Deletion of Dicer1 in the Sertoli cell lineage at 13.5 days post coitum (dpc), using We have screened previously the small RNA population of differentiating XY and XX gonads using high-throughput sequencing to identify microRNAs that may regulate mouse embryonic gonad development . We detected the microRNAs miR- 140-5p/miR-140-3p as being expressed in differentiating testes.…”

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confidence: 99%

Section: Introductionmentioning

confidence: 99%

The role of signalling pathways in urogenital ridge differentiation

Wainwright¹

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First, the function of the ROBO2-SLIT2 pathway in patterning the kidney domain in the early urogenital ridge was examined. Loss of Robo2 in mouse and human is known to result in the formation of supernumerary kidneys driven by an expansion of Gdnf expression. Examination of the early urogenital ridge revealed that the number of cells in the nephrogenic cord was increased in Robo2-null mice, resulting in ectopic caudal mesonephric tubules and an expanded metanephric mesenchyme. In addition, the metanephric mesenchyme fails to separate from the Wolffian duct during kidney development, suggesting that the morphogenesis of the metanephric mesenchyme away from the Wolffian duct may result from active cell migration.Second, the anterior-posterior extension of the intermediate mesoderm and the upper and lower urinary tract differentiation was investigated in Wnt5a-null mice. It was observed that Wnt5a-null mice develop a horseshoe kidney. Underlying horseshoe kidney formation, Wolffian duct migration and insertion into the cloaca are disrupted in Wnt5a-null mice. These defects were reminiscent of mice with perturbed retinoic acid signalling, which led to the finding that the Wolffian duct is exposed to abnormally high levels of retinoic acid in Wnt5a-null mice. Therefore, the likely underlying cause of Wolffian duct migration defects in Wnt5a-null mice is exposure to increased retinoic acid concentrations, secondary to the failure of global axis extension. iv Third, the anterior-posterior extension of the gonad domain in intermediate mesoderm patterning was investigated by studying mouse mutants with a defect in retrograde trafficking of primary cilia.Mouse mutants of the primary cilium component Ift144, develop XY and XX gonads that are larger than wild-type. Investigation of the early patterning of the urogenital ridge found the anteriorposterior domain of the gonad was extended with a concomitant extension of the embryo trunk axis.Extension of the anterior-posterior gonad axis resulted in an increase in testis cord number, suggesting that the gonad domain is partitioned along the available space rather than partitioned a finite number of times. In addition, somitogenesis in the trunk of the embryo was disrupted, with somitogenesis in the tail proceeding correctly, suggesting that perturbed somite segmentation may be the cause of the increased trunk extension. Thus, analysis of Ift144 mouse mutants has suggested that the length of the trunk axis of the embryo is the main determinant of the gonad anteriorposterior domain and helped to clarify the paradigm of testis cord formation.Fourth, the expression, regulation and function of the microRNA miR-202 was examined in testis differentiation. miR-202-5p/3p was detected as being expressed specifically in the Sertoli cells, during XY gonad differentiation. Over-expression of pri-miR-202 in XX gonads did not perturb XX gonad differentiation, suggesting that pri-miR-202 does not directly antagonize the XX differentiation pathway. Furthermore, investigation of the pri...

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Inactivation of Dicer1 has a severe cumulative impact on the formation of mature germ cells in mouse testes

Cited by 28 publications

References 33 publications

MicroRNAs 221 and 222 regulate the undifferentiated state in mammalian male germ cells

MicroRNAs 221 and 222 regulate the undifferentiated state in mammalian male germ cells

Role of microRNAs in spermatogenesis

The role of signalling pathways in urogenital ridge differentiation

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