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During nondisjunction, homologous chromosomes or sister chromatids fail to separate correctly and both move to the same pole instead of opposite poles. This produces daughter cells with abnormal chromosome numbers—some cells receive extra chromosomes while others lack them entirely, resulting in aneuploid gametes.

Nondisjunction occurs during anaphase I or anaphase II of meiosis. In anaphase I, homologous chromosome pairs fail to detach and separate. In anaphase II, sister chromatids remain attached and move to the same pole instead of separating to opposite poles.

Nondisjunction during anaphase I results from mutations in synaptonemal complex proteins that normally hold homologous chromosomes together, asymmetric spindle fibers, or chromosome misorientation. These defects prevent proper chromosome detachment and separation to opposite poles.

Nondisjunction during anaphase II arises from defects in topoisomerase II or condensins, proteins essential for separating sister chromatids. When these proteins malfunction, sister chromatids remain attached and move together to the same pole instead of separating.

When a gamete with abnormal chromosomes from nondisjunction fertilizes a normal gamete, the resulting zygote has an abnormal chromosome number, causing aneuploidy. This produces monosomy (2n-1) with fewer chromosomes or trisomy (2n+1) with extra chromosomes, such as Down Syndrome or Turner Syndrome.

The transcript and overview content do not provide specific mechanistic explanations for why nondisjunction occurs more frequently during oogenesis compared to spermatogenesis. This difference is noted but the underlying biological reasons are not detailed in the source material.

Nondisjunction produces four haploid daughter cells with unequal chromosome distribution. Two cells receive an additional chromosome while two cells lack a chromosome. This creates aneuploid gametes that, when fertilized, can result in offspring with chromosomal abnormalities like monosomy or trisomy.