In December 2019, a severe respiratory disease was first appeared in Wuhan, China and has now spread to many countries and affected many people around the world (WHO, 2020). This pandemic disease was named coronavirus disease 2019 (COVID-19) by the World Health Organization (WHO) and was found to be caused by a novel virus belongs to the family Coronaviridea (WHO, 2020; Zhou et al., 2020). Because of the high homology with the Severe Acute Respiratory Syndrome Corona Virus (SARS-CoV), the novel virus was named as Severe Acute Respiratory Syndrome Corona Virus-2 SARS-CoV-2 (Zhu, Zhang, et al., 2020). Coronaviruses have caused large health epidemics in the past, as SARS-CoV caused a health epidemic in 2003, and another large-pandemic outbreak caused by the Middle-East Respiratory Syndrome CoronaVirus (MERS-CoV) in 2012 (reviewed in Di Mascio et al., 2020). SARS-CoV and SARS-CoV-2 recognise the same human cell receptor; angiotensin-converting enzyme 2 (ACE2), while MERS-CoV binds to a different receptor called dipeptidyl peptidase 4 DPP4
Male infertility is commonly associated with sperm abnormalities including asthenozoospermia. The molecular basis of asthenozoospermia was linked to mitochondrial DNA (mtDNA) mutations. The 4,977‐bp human mtDNA deletion is one of the most common mutations of spermatozoa and results in loss of about 33% of the mitochondrial genome. In this preliminary study, we aimed to investigate the presence of 4,977‐bp mtDNA deletion in asthenozoospermic infertile men in Jordan. Semen specimens of 120 asthenozoospermic infertile men and 80 normozoospermic individuals were collected at the in vitro fertilization unit. MtDNA was extracted after the enrichment of spermatozoa; then, polymerase chain reaction was performed using 4,977‐bp mtDNA deletion‐specific primers. The deletion of 4,977‐bp mtDNA was detected in 79.2% of asthenozoospermic patients compared to 10% in normozoospermic controls. The results showed a significant association between the presence of 4,977‐bp mtDNA deletion and the asthenozoospermia and infertility (OR = 34.2000, 95% CI = 14.57–80.26, p‐value < .001). In conclusion, our findings underscored a strong association between 4,977‐bp mtDNA deletion and asthenozoospermia in the Jordanian population.
Assisted reproductive technology is a common procedure which helps millions of couples who suffer fertility problems worldwide every year. Screening for genetic abnormalities prior to such procedure is very important to prevent the transmission of harmful genetic mutations to future generations. Microdeletions within the azoospermia factor (AZF) region of the Y chromosome and the expansion of the CAG trinucleotides in the androgen receptor (AR) gene are among the susceptible causes of male infertility in different ethnic groups. Such association has never been studied in Jordan. In this study, we compared CAG repeat length between azoospermic infertile and normospermic fertile Jordanian males and we also screened the frequency of Y chromosome microdeletions in the same cohort. The study included 142 nonobstructive azoospermic cases and 145 normospermic controls. Results have shown that the median CAG repeat length in the azoospermic group is 19 ± 2 compared to 19 ± 1.5 (p = .6262) in the control group. Deletions within the Y chromosome AZF region were detected in 7 of 142 cases (4.93%) and no deletions were seen in the control group. The results of this study confirm the importance of the AZF region in normal spermatogenesis, whereas it shows no link between the length of CAG repeats in the AR gene and male azoospermia in Jordanian group examined.
Chromosome segregation in meiosis is controlled by a conserved pathway that culminates in Separase-mediated cleavage of the α-kleisin Rec8, leading to dissolution of cohesin rings. Drosophila has no gene encoding Rec8, and the absence of a known Separase target raises the question of whether Separase and its regulator Securin (Pim in Drosophila) are important in Drosophila meiosis. Here, we investigate the role of Securin, Separase and the cohesin complex in female meiosis using fluorescence in situ hybridization against centromeric and arm-specific sequences to monitor cohesion. We show that Securin destruction and Separase activity are required for timely release of arm cohesion in anaphase I and centromere-proximal cohesion in anaphase II. They are also required for release of arm cohesion on polar body chromosomes. Cohesion on polar body chromosomes depends on the cohesin components SMC3 and the mitotic α-kleisin Rad21 (also called Vtd in Drosophila). We provide cytological evidence that SMC3 is required for arm cohesion in female meiosis, whereas Rad21, in agreement with recent findings, is not. We conclude that in Drosophila meiosis, cohesion is regulated by a conserved Securin-Separase pathway that targets a diverged Separase target, possibly within the cohesin complex.
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