You will be presented with the full text of a biomedical research paper. Please write an abstract for this paper. Your response should include the abstract and no additional text.

Paper text:
in meiosis , reciprocal recombination , also known as crossing over or chiasma formation , plays the vital role of holding homologous chromosomes together until their proper segregation at the first meiotic division . in human females
it has long been known that either the failure of a pair of homologs to recombine , or an unusual distribution of recombination events , is associated with meiotic nondisjunction .
these observations have led to a two - step model of meiotic nondisjunction in which the creation of so - called  vulnerable crossover configurations during meiotic prophase ( a process that occurs during mid - to - late - fetal development in human beings ) predisposes homologs to nondisjoin at either the first or second meiotic division events ( events that occur one to five decades later ) [ 2 - 4 ] . given that crossovers function by virtue of using sister - chromatid cohesion on both sides of the crossover to link the homologs together
, it makes sense that either the failure of crossing over per se or a crossover that occurred too distally between a pair of homologs might have insufficient cohesion to ensure proper homolog segregation .
one prediction of this model is that these vulnerable crossover configurations do exist in fetal oocytes .
this proposal has recently been directly tested and the results are described in a paper by cheng et al .
cheng et al . studied the localization of the crossover associated protein mlh1 ( for a review , see ) in more than 1000 prophase oocytes derived from 31 fetal ovarian samples .
although their studies did indeed confirm the existence of the predicted vulnerable crossover configurations ( i.e. , either a pair of homologs with no detectable mlh1 foci or bivalents with only a very distal or proximal focus ) , there were several unexpected observations .
first , their observations confirm those of others   in suggesting that crossing over occurs over a wider temporal window in human females ( from zygotene to pachytene ) than it does in either human males or mouse females ( where mlh1 foci appear to be tightly restricted to pachytene ) .
second , the number of mlh1 foci observed predicts a total genome genetic length of only 3465 cm , some 80% of the value of 4300 - 4600 cm obtained from direct measurement by linkage studies ( for a review , see ) .
as pointed out by the authors , the most reasonable explanation for this discrepancy is because crossover formation occurs over a wide temporal window , and some events may , therefore , be completed before others are initiated and it may thus not be possible to visualize all mlh1 foci that occur in a given oocyte at a single time .
in addition , holloway et al .   have provided strong evidence in mouse oocytes for a set of mlh1-independent crossovers mediated via the mus81 pathway . moreover , using high - resolution linkage analysis in humans , fledel - alon et al .  
have demonstrated the existence of double crossovers that occur in surprisingly close proximity , and suggested that one or both of these crossovers might be mediated by an mlh1-independent second pathway .
thus , the deficit of mlh1 foci , with respect to the length of the genetic map , may well be explained both by the fact that not all mlh1 foci are seen at any one time and by the existence of a second mlh1-independent pathway for crossing over . however , there is a more serious discrepancy with respect to vulnerable crossover configurations .
have estimated that the frequency of oocytes lacking a crossover on chromosome 13 is close to 12% and oliver et al .  
have determined that the frequency of oocytes that are non - exchange for chromosome 21 is approximately 20% .
similar data for chromosome 21 derived from high - resolution recombination mapping have been recently published by fledel - alon et al . . these values are substantially higher than the values of 1% ( chromosome 13 ) and 4.9%
thus , the frequency of non - crossover oocytes for both chromosome 21 and chromosome 13 , as estimated by linkage analysis , significantly exceeds the fraction of nonexchange chromosomes as measured by the absence of mlh1 foci . as cheng et al .
point out , these discrepancies are extremely hard to understand . one component of the difference may be methodological  it is standard practice in these types of cytological studies to ignore oocytes with obvious failures in pairing and synapsis .
perhaps some of these oocytes contribute to the pool of functional oocytes on which linkage studies are based .
the authors best attempt to reconcile these disparate observations is to note that their estimates of non - exchange bivalents provide a better fit for the frequency of aneuploid embryos , assuming that all non - exchange bivalents segregate their homologs at random .
unfortunately , this assumption ignores the possibility that , like many other organisms [ 13 - 15 ] , human females may indeed possess an exchange - independent back - up system for ensuring the segregation of those chromosomes that fail to recombine .
the study by cheng et al . offers intriguing insights into the distribution of mlh1 foci , and their temporal control in human fetal oocytes . of even greater interest
are the authors observations regarding the nature of interference in human oocytes and differences in the types of unusual ( and presumably vulnerable ) crossover distributions observed for different human chromosomes .
one size fits all model for explaining the effects of abnormalities in recombination distribution on proper segregation .
that said , the dilemma of just how many non - crossover bivalents there really are , and to what degree various classes of crossover and non - crossover bivalents might be selected for or against during oocyte development , remains open - as does the issue of whether or not human females may indeed have a system for ensuring the segregation of non - crossover bivalents ( a possibility that would , quite honestly , not surprise this author ) .
but perhaps most importantly , the observations of cheng et al . and those of others ( for example , see ) need to be viewed as a starting point - one in which prophase human oocytes become accessible to the types of analysis of crossover events , as defined by location of the proteins such as mlh1 , which are routinely applied to human male meiotic cells and mouse oocytes .
surely , further study of the recombination process in human oocytes will address the questions asked above .
the nature of the relationship between crossing over and failed segregation in human oocytes is of obvious interest . 
 a recent paper by cheng and colleagues provides important insights into the distribution of crossover events ( as marked by mlh1 foci ) in human oocytes and raises complex questions regarding discrepancies between direct cytological assessment of exchange and measurement of crossing over by linkage analysis .