The dynein-related genes may have a role in the etiology of male infertility, particularly in cases of impaired sperm motility.
The goal of this review is to compile a list of the most important dynein-related candidate genes that may contribute to male factor infertility.
Databases were searched using the keywords \"dynein,\" \"male,\" \"infertility,\" and by applying strict inclusion criteria. A meta-analysis was also performed by using the eligible case-control studies. The odd ratios (ORs), the Z-test score, and the level of significance were determined using a fixed model with a p value of 0.05. Funnel plots were used to check for publication bias.
There were 35 studies that met the inclusion criteria. There were a total of 15 genes responsible for the production of dynein structural proteins, the production of dynein assembling factors, and potentially associated with male infertility. A total of five case-control studies were eligible for inclusion in the meta-analysis. Variants in the dynein-related genes were linked to an increased the risk of male infertility (OR = 21.52, 95% confidence interval 8.34-55.50, Z test = 6.35, p < 0.05). The percentage of heterogeneity, I2 , was 47.00%. The lack of variants in the dynein genes was an advantage, and this was statistically significant.
The results from the present review illustrate that pathogenic variants in genes both for dynein synthesis and for dynein assembly factors could be associated with isolated cases of male infertility without any other symptoms.
The genes addressed in this study, which are involved in both the production and assembly of dynein, could be used as molecular targets for future research into the etiology of sperm motility problems.

Dyneins are multiprotein complexes that move cargo along microtubules in the minus end direction. The largest individual component of the dynein complex is the heavy chain. Its C-terminal 3500 amino-acid residues form the motor domain, which hydrolyses ATP in its ring of AAA+ (ATPases associated with diverse cellular activities) domains to generate the force for movement. The production of force is synchronized with cycles of microtubule binding and release, another important prerequisite for efficient motility along the microtubule. Although the large scale conformational changes that lead to force production and microtubule affinity regulation are well established, it has been largely enigmatic how ATP-hydrolysis in the AAA+ ring causes these rearrangements. The past five years have seen a surge of high resolution information on the dynein motor domain that finally allowed unprecedented insights into this important open question. This review, part of the \"ATP and GTP hydrolysis in Biology\" special issue, will summarize our current understanding of the dynein motor mechanism with a special emphasis on the recently obtained crystal and EM structures. © 2016 Wiley Periodicals, Inc. Biopolymers 105: 557-567, 2016.