Abstract:The term “Puberty”, socially known as “Adolescence” is the transitional period from juvenile life to adulthood with functional maturation of gonads and genital organs. In this process, some remarkable developmental changes occur in morphology, physiology, and behavior leading to reproductive competence. Despite sufficient levels of gonadotropins (luteinizing hormone [LH] and follicle‐stimulating hormone [FSH]), robust spermatogenesis is not initiated during infancy in primates due to the immaturity of testicul… Show more
“…This is a tightly regulated asynchronized process, broadly sub-divided into four major developmental stages, namely, 1) pre-meiotic proliferation of undifferentiated spermatogonia, 2) meiotic entry of differentiated spermatogonia 3) meiotic completion and formation of round spermatid, and 4) maturation of elongated spermatid to spermatozoa ( Griswold, 2016 ). Testicular Sertoli cells (Sc) provide the structural and biochemical support to all the stages of male Gc within the seminiferous tubules ( Griswold, 2018 ; Bhattacharya et al, 2019 ). Both Gc-specific intrinsic and Sc-derived extrinsic factors collectively determine the Gc developmental fate ( Griswold, 2018 ; Bhattacharya et al, 2019 ).…”
Section: Introductionmentioning
confidence: 99%
“…Testicular Sertoli cells (Sc) provide the structural and biochemical support to all the stages of male Gc within the seminiferous tubules ( Griswold, 2018 ; Bhattacharya et al, 2019 ). Both Gc-specific intrinsic and Sc-derived extrinsic factors collectively determine the Gc developmental fate ( Griswold, 2018 ; Bhattacharya et al, 2019 ).…”
Germ cells (Gc) propagate the genetic information to subsequent generations. Diploid (2n) Gc get transformed to specialized haploid (n) gametes by mitotic and meiotic divisions in adult gonads. Retinoic acid (RA), an active derivative of vitamin A (retinol), plays a critical role in organ morphogenesis and regulates the meiotic onset in developing Gc. Unlike ovaries, fetal testes express an RA-degrading enzyme CYP26B1, and thereby, male Gc fail to enter into meiosis and instead get arrested at G0/G1 stage, termed as gonocytes/pro-spermatogonia by embryonic (E) 13.5 days. These gonocytes are transformed into spermatogonial stem/progenitor cells after birth (1–3 days of neonatal age). During post-natal testicular maturation, the differentiating spermatogonia enter into the meiotic prophase under the influence RA, independent of gonadotropic (both FSH and LH) support. The first pulse of RA ensures the transition of undifferentiated type A spermatogonia to differentiated A1 spermatogonia and upregulates STRA8 expression in Gc. Whereas, the second pulse of RA induces the meiotic prophase by augmenting MEIOSIN expression in differentiated spermatogonia B. This opinion article briefly reviews our current understanding on the RA-driven spermatogonial differentiation in murine testes.
“…This is a tightly regulated asynchronized process, broadly sub-divided into four major developmental stages, namely, 1) pre-meiotic proliferation of undifferentiated spermatogonia, 2) meiotic entry of differentiated spermatogonia 3) meiotic completion and formation of round spermatid, and 4) maturation of elongated spermatid to spermatozoa ( Griswold, 2016 ). Testicular Sertoli cells (Sc) provide the structural and biochemical support to all the stages of male Gc within the seminiferous tubules ( Griswold, 2018 ; Bhattacharya et al, 2019 ). Both Gc-specific intrinsic and Sc-derived extrinsic factors collectively determine the Gc developmental fate ( Griswold, 2018 ; Bhattacharya et al, 2019 ).…”
Section: Introductionmentioning
confidence: 99%
“…Testicular Sertoli cells (Sc) provide the structural and biochemical support to all the stages of male Gc within the seminiferous tubules ( Griswold, 2018 ; Bhattacharya et al, 2019 ). Both Gc-specific intrinsic and Sc-derived extrinsic factors collectively determine the Gc developmental fate ( Griswold, 2018 ; Bhattacharya et al, 2019 ).…”
Germ cells (Gc) propagate the genetic information to subsequent generations. Diploid (2n) Gc get transformed to specialized haploid (n) gametes by mitotic and meiotic divisions in adult gonads. Retinoic acid (RA), an active derivative of vitamin A (retinol), plays a critical role in organ morphogenesis and regulates the meiotic onset in developing Gc. Unlike ovaries, fetal testes express an RA-degrading enzyme CYP26B1, and thereby, male Gc fail to enter into meiosis and instead get arrested at G0/G1 stage, termed as gonocytes/pro-spermatogonia by embryonic (E) 13.5 days. These gonocytes are transformed into spermatogonial stem/progenitor cells after birth (1–3 days of neonatal age). During post-natal testicular maturation, the differentiating spermatogonia enter into the meiotic prophase under the influence RA, independent of gonadotropic (both FSH and LH) support. The first pulse of RA ensures the transition of undifferentiated type A spermatogonia to differentiated A1 spermatogonia and upregulates STRA8 expression in Gc. Whereas, the second pulse of RA induces the meiotic prophase by augmenting MEIOSIN expression in differentiated spermatogonia B. This opinion article briefly reviews our current understanding on the RA-driven spermatogonial differentiation in murine testes.
“…1 ) [ 20 – 22 ]. Pseudo-aligners were introduced more recently and therefore have lower adoption but are beginning to see wider usage [ 23 , 24 ]. Fig.…”
Background
Full-length isoform quantification from RNA-Seq is a key goal in transcriptomics analyses and has been an area of active development since the beginning. The fundamental difficulty stems from the fact that RNA transcripts are long, while RNA-Seq reads are short.
Results
Here we use simulated benchmarking data that reflects many properties of real data, including polymorphisms, intron signal and non-uniform coverage, allowing for systematic comparative analyses of isoform quantification accuracy and its impact on differential expression analysis. Genome, transcriptome and pseudo alignment-based methods are included; and a simple approach is included as a baseline control.
Conclusions
Salmon, kallisto, RSEM, and Cufflinks exhibit the highest accuracy on idealized data, while on more realistic data they do not perform dramatically better than the simple approach. We determine the structural parameters with the greatest impact on quantification accuracy to be length and sequence compression complexity and not so much the number of isoforms. The effect of incomplete annotation on performance is also investigated. Overall, the tested methods show sufficient divergence from the truth to suggest that full-length isoform quantification and isoform level DE should still be employed selectively.
“…12 The functional maturation of Scs during puberty directs the robust initiation of first spermatogenic wave, whereas the final number of Scs in the pubertal testes determines the maximal spermatogenic output. 17,44,45 MicroRNAs are well-established transacting factors for optimizing developmental gene expression in various cellular processes, including gonadal differentiation. Several studies have shown microRNAs like miR-34/449, miR-10a, miR-100-3p, miR-383, etc., to be crucial for mammalian spermatogenesis.…”
A major change in the transcriptome of testicular Sertoli cells (Scs) at the onset of puberty enables them to induce robust spermatogenesis. Through comprehensive literature mining, we generated a list of genes crucial for Sc functioning and computationally predicted the microRNAs regulating them. Differential expression analysis of microRNAs in infant and pubertal rat Scs showed that miR-382-3p levels decline significantly in pubertal Scs. Interestingly, miR-382-3p was found to regulate genes like Ar and Wt1, which are crucial for functional competence of Scs. We generated a transgenic (Tg) mouse model in which pubertal decline of miR-382-3p was prevented by its overexpression in pubertal Scs. Elevated miR-382-3p restricted the functional maturation of Scs at puberty, leading to infertility. Prevention of decline in miR-382-3p expression in pubertal Scs was responsible for defective blood-testis barrier (BTB) formation, severe testicular defects, low epididymal sperm counts and loss of fertility in these mice. This provided substantial evidence that decline in levels of miR-382-3p at puberty is the essential trigger for onset of robust spermatogenesis at puberty. Hence, sustained high levels of miR-382-3p in pubertal Scs could be one of the underlying causes of idiopathic male infertility and should be considered for diagnosis and treatment of infertility.
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