Evidence map›Paper›PMID 33766143›Full record

ReviewCell & bioscience2021

Human AZFb deletions cause distinct testicular pathologies depending on their extensions in Yq11 and the Y haplogroup: new cases and review of literature.

P H Vogt, U Bender, B Deibel, F Kiesewetter, J Zimmer, T Strowitzki

Open access · goldAbstract readReview
In one paragraph

Review in Cell & bioscience, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
3.1field-weighted citation impact, top 8% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

11 citing papers in PubMed, 25 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Review
  5. Review
  6. Article
  7. Article
  8. Microenvironment for spermatogenesis and sperm maturation.Histochemistry and cell biology · 2022
    Review
  9. Review
  10. Repetitive DNA Sequences in the Human Y Chromosome and Male Infertility.Frontiers in cell and developmental biology · 2022
    Review
  11. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

6 authors at 2 institutions in 1 country.

P H VogtDivision of Reproduction Genetics, Department of Gynaecol. Endocrinology & Infertility Disorders, Women Hospital, University of Heidelberg, Im Neuenheimer Feld 440, 69120, Heidelberg, Germany. peter.vogt@med.uni-heidelberg.de.
U BenderDivision of Reproduction Genetics, Department of Gynaecol. Endocrinology & Infertility Disorders, Women Hospital, University of Heidelberg, Im Neuenheimer Feld 440, 69120, Heidelberg, Germany.
B DeibelDivision of Reproduction Genetics, Department of Gynaecol. Endocrinology & Infertility Disorders, Women Hospital, University of Heidelberg, Im Neuenheimer Feld 440, 69120, Heidelberg, Germany.
F KiesewetterDepartment of Andrology, University Clinic of Dermatology, Erlangen, Germany.
J ZimmerDivision of Reproduction Genetics, Department of Gynaecol. Endocrinology & Infertility Disorders, Women Hospital, University of Heidelberg, Im Neuenheimer Feld 440, 69120, Heidelberg, Germany.
T StrowitzkiDepartment of Gynaecol. Endocrinology & Infertility Disorders, Women Hospital, University of Heidelberg, Heidelberg, Germany.
Heidelberg University · DEUniversitätsklinikum Erlangen · DE

Funding

Deutsche Forschungsgemeinschaft Vo403/12-1
6 · The paper itself

Abstract

Genomic AZFb deletions in Yq11 coined "classical" (i.e. length of Y DNA deletion: 6.23 Mb) are associated with meiotic arrest (MA) of patient spermatogenesis, i.e., absence of any postmeiotic germ cells. These AZFb deletions are caused by non-allelic homologous recombination (NAHR) events between identical sequence blocks located in the proximal arm of the P5 palindrome and within P1.2, a 92 kb long sequence block located in the P1 palindrome structure of AZFc in Yq11. This large genomic Y region includes deletion of 6 protein encoding Y genes, EIFA1Y, HSFY, PRY, RBMY1, RPS4Y, SMCY. Additionally, one copy of CDY2 and XKRY located in the proximal P5 palindrome and one copy of BPY1, two copies of DAZ located in the P2 palindrome, and one copy of CDY1 located proximal to P1.2 are included within this AZFb microdeletion. It overlaps thus distally along 2.3 Mb with the proximal part of the genomic AZFc deletion. However, AZFb deletions have been also reported with distinct break sites in the proximal and/or distal AZFb breakpoint intervals on the Y chromosome of infertile men. These so called "non-classical" AZFb deletions are associated with variable testicular pathologies, including meiotic arrest, cryptozoospermia, severe oligozoospermia, or oligoasthenoteratozoospermia (OAT syndrome), respectively. This raised the question whether there are any specific length(s) of the AZFb deletion interval along Yq11 required to cause meiotic arrest of the patient's spermatogenesis, respectively, whether there is any single AZFb Y gene deletion also able to cause this "classical" AZFb testicular pathology? Review of the literature and more cases with "classical" and "non-classical" AZFb deletions analysed in our lab since the last 20 years suggests that the composition of the genomic Y sequence in AZFb is variable in men with distinct Y haplogroups especially in the distal AZFb region overlapping with the proximal AZFc deletion interval and that its extension can be "polymorphic" in the P3 palindrome. That means this AZFb subinterval can be rearranged or deleted also on the Y chromosome of fertile men. Any AZFb deletion observed in infertile men with azoospermia should therefore be confirmed as "de novo" mutation event, i.e., not present on the Y chromosome of the patient's father or fertile brother before it is considered as causative agent for man's infertility. Moreover, its molecular length in Yq11 should be comparable to that of the "classical" AZFb deletion, before meiotic arrest is prognosed as the patient's testicular pathology.

Indexed as

AZFb-c ampliconsAZFb “de novo” and “polymorphic” deletionsAZFb Y genes“Classical” and “non-classical” AZFb deletionsMeiotic arrestOAT syndromeY-haplogroups

Identifiers

PMID33766143
PMCPMC7995748
OpenAlexW3139402128

What OpenQuestion holds

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.