Genes related to defects in Meiosis
Genes associated with spermatogenic arrest
Genes related to sperm-egg interaction
Genes related to sperm structure
Gene Phenotype References
Cyclin A1 meiotic arrest prior to first division, increased apoptosis Liu et al, 1998
Cyclin D2 decreased sperm concentration Sicinski et al, 1996
DMC1 meiotic arrest at zygotene, abnormal synaptonemal complex Pittman et al, 1998
HSP 70-2 synaptonemal comples fails to desynapse Dix et al, 1997
MLH1 meiotic pachytene arrest Baker et al, 1996
MSH4 abnormal chromosome pairing during zygotene Kneitz et al, 2000
MSH5 incorrect or absent chromosomal pairing Edelmann et al, 1999
PMS2 partial meiotic arrest, oligo- teratozoospermia Baker et al, 1995
SCP3 failure of synaptonemal complex to form Yuan et al, 2000
TLS delayed, unpaired and mispaired chromosomes Kuroda et al, 2000
A-myb degeneration of primary spermatocytes Toscani et al, 1997
BCL-w increased apoptosis Print et al, 1998
Crem round spermatid stage arrest Blendy et al, 1996
DAZl speramatogonial arrest Ruggiu et al, 1997
Morc increased apoptosis, prophase 1 arrest Watson et al, 1998
Spermine synthase build up of spermidine, spermatogenic arrest Lorenz et al, 1998
TRF-2 speramatogonial arrest Zhang et al, 2001
Vasa depletion of post meiotic germ cells Tanaka et al, 2000
no sperm-egg adhesion, poor transit through
Ikawa et al, 1997
Cyritestin sperm fail to bind zona pellucida Shamsadin et al, 1999
Fertilin B same as calmegin Cho et al, 2000
CK2 oligo- and globozoospermia Xu et al, 1999
C-ros bent tails and decreased motility Yeung et al, 1999
EGR4 multiple structural abnormalities
Tourtellotte et al,
E-map-115 deformed nuclei, abnormal microtubule associations Komada et al, 2000
JunD oligo- astheno- teratozoospermia Thepot et al, 2000
nectin-2 misshapen heads and midpieces Bouchard et al, 2000
PCI abnormal morphology and fertilization Uhrin et al, 1999
THEG abnormal elongation and tail defects Yanaka et al, 2000
Tumour of penis and prepuce
Infection of vas deferens and ampulla
Lack of condition or obese condition
Torsion or rotation of descended testis
Improper delivery of semen
Fistulous opening of urethra
1- Reduced or complete lack of sexual desire and ability
to copulate (Impotentia Coeundi).
2- Inability or reduced ability to fertilize (Impotentia
3- Miscellaneous Diseases affecting reproductive organs
Reduced to complete lack of sexual desire and ability
In males complete physical capability is necessary so
that each component of copulatory patterns (sexual
arousal, sexual display, erection, protrusion, mounting,
intromission and dismounting) are performed well.
Necessary for males that all senses (visual, olfactory,
auditory and tactile) should be perfectly normal.
Incapacity or reduced capacity to fertilize.
Characterized by normal sexual desire as well as
normal ability to copulate but fertility is either
subnormal or absent.
1- Associated with production of apparently normal
May be due to:
a) Infectious diseases
b) Inherited sperm defects.
2- Associated with production of semen, which is
abnormal in morphology, concentration, motility, and
• IBR-IPV etc.
Semen may be normal in motility, conc., and morphology
but such semen results in embryonic/foetal death,
abortion, and signs of infertility.
Inherited sperm defects
• Diadem defect/nuclear pouch formation
defect/eversion of galea capitis and crater shaped
Sign of severe disturbance in spermiogenesis rendering a
bull infertile or nearly sterile. There are invaginations
of the nuclear membrane and defect is confined near
anterior border of the post nuclear cap. Feulgen stain
and phase contrast microscopy reveal this defect.
• Knobbed spermatozoa
Acrosomal defect related to defective spermiogenesis
involving golgi apparatus. Eosin-B, fast green or
phase contrast microscopy reveal this defect. Sperm
incapable of penetrating ovum.
• Gene or chromosomal defects
Occurs at meiosis due to chromosomal aberration.
Structural changes of chromosomes including
translocation and inversion. May cause fertilization but
zygote dies in early gestation.
Knobbed spermatozoa Gene or chromosomal defects
• Atypical basic nuclear proteins
Defect in sperm cell chromatin. Interfere with activation
and penetration of sperm into ova.
• Inherent enzymatic disturbances
Causes early death of spermatozoa in female genital
This type of infertility may be associated with pathology
of testes, epididymis, vas deferens, accessory sex
glands and urethra or may be associated with abnormal
semen production due to congenital or heriditary causes
or due to acquired causes.
Imperfect descent of testis
Scrotal or inguinal hernia
Tumours of epididymis
Segmental aplasia of mesonephric duct
Pathology of vas deferens and ampulla
Inherited or congenital sperm cell defects
Ultrastructure abnormality in neck or implantation region
of sperm resulting disintegration into heads and tails in
caput of epididymis.
Sterilizing tail stump
Instead of actual tail, there is a short tail stump(2-3µ)
Main piece strongly coiled over mid piece. In about 40%
spermatozoa. Found associated with elevated levels of
zinc in seminal plasma.
Pseudo droplet defect
Sperm have rounded or elongated thickening on mid
Sterilizing tail stump Pseudo droplet defect Dag defect
Cork screw defect
Mid piece in shape of corkscrew due to irregular
distribution of mitochondrial sheath.
Returned tail and narrow head
Apparently genetic found in jersey breed.
Results in reduced fertility accompanied by increase in
the number of abnormal seminiferous tubules,poor
semen quality and testicular hypoplasia.
Infertility in hybrids
Major difference in number of chromosomes of parents
leads to infertility in offspring. Sterility common in
male hybrids. Eg Horse and ass crosses (mule sterile),
bison and domestic cattle (bulls sterile), yak and
domestic cattle (bulls sterile) etc.
Animals with congenital malformation of sexual development
rendering them invariably sterile.
• True hermaphrodites: have various combinations of ovaries,
testis and ovo-testis together with varying of bisexuality in
accessory sex organs.
• Male and female pseudo-hermaphrodites: exists
discrepancy between external genetalia and gonads. Males
have testis and female externalia and females have ovaries
and male externalia.
• Freemartins : results from sexual modification of female
twin due to exchange of blood from male twin in uterus.
Torsion or rotation of testis
Testicles rotated and held high in scrotum. Semen
characteristics not affected but spermatozoa production
Glans penis have opening on ventral side leading to
deposition of semen in middle of vagina.
Necrosis or lodgement of calculi in urethral process leads
to improper delivery of semen.
Some male animals have high fertility but show low
fertility and the cause remains unexplained.
Fertility is determined genetically.
The semen of some male animals do not withstand
The fertility of male animals also varies from herd to
herd and from individual to individual and also in the
same individual at different times.
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Presentation about male animal infertility types and causes.