As reported from (Table 1) deficient heterozygotes appears to impact strong response to progressive inbreeding, genetic hitch-hiking, the presence of null alleles
and population sub-structures seemed to enforced lowered heterozygous conditions (Nei, 1987).
The results of this study are comparable to our findings, however, the patients included in the study were all under 25 years of age.23 A meta-analysis comprising 23 studies from different Asian countries illustrated significant association of GST null polymorphisms with acute leukemia risk in children while no association with adults.24 This difference in results depict geographic variations in GST null allele
distribution and its association with ALL.
Although the present samples do not allow for examination of Mendelian inheritance of the microsatellite alleles, the results indicate that the deficiency of heterozygotes at MaF214 and OarFCB304 microsatellites could be due to the presence of non-amplifying null alleles
. Positive f estimates for 2 studied microsatellites could be assumed as an indication for inbreeding.
All mismatches, however, were found at homozygous loci where occurrence of null allele
cannot be excluded.
The departures in segregation pattern from the expected ratio, which was observed for the Ccmic3 locus in Families A1 and A7, were initially thought to be caused by the presence of a null allele
. Analysis of the progeny revealed 2 improbable Mendelian ratios for both these crosses (A3 expected 1:1, A3 observed 1:2:1; A7 expected 1, A7 observed 1:1; Table 4).
On the other hand, result of [F.sub.(null)] and frequency of null allele
indicate some populations contain substantial proportion of null alleles
and this also contributed to the excessive homozygosity.
Mice with two SOX5 null alleles
die in the early postnatal period  and their brains show severe defects in the generation of neuronal subcortical projections .
Identification of a null allele
at the Wx-B1 locus in some of Iranian bread wheat genotypes, Advances in Environmental Biology, 6(10): 2586-2589.
The results of the analysis of polymorphisms in GSTM1 and GSTT1 indicated that there was a higher incidence of the GSTM1 null allele
of 66.7% in the nonsmokers group compared to 43.4% with the GSTM1 null allele
in the smokers group.
The much stronger phenotype observed when the [Ubx.sup.1] null allele
is in trans with [Ubx.sup.CPTI000601] supports the view that the protein trap allele has reduced Ubx function and is thus a weak hypomorph.
Wx-B1 null allele
indicates reduced amylase (Briney et al., 1998).