Journal of Heredity Advance Access originally published online on July 12, 2006
Journal of Heredity 2006 97(4):417-422; doi:10.1093/jhered/esl014
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
PRINS-Labeled Knobs Are Not Associated with Increased Chromosomal Stickiness in the Maize st1 Mutant
From the Department of Crop Sciences, University of Illinois, 1201 W. Gregory Dr., 360 ERML, Urbana, IL 61801
Address correspondence to A. L. Rayburn at the address above, or e-mail: arayburn{at}uiuc.edu.
In maize, the st1 mutant has been observed to result in chromosomes that stick together during both mitotic and meiotic anaphase. These sticky chromosomes result in abnormal chromosome separation at anaphase. Although the mechanism producing the st1 mutant phenotype is unknown, delayed replication of knob heterochromatin has been implicated in similar phenomena that result in sticky chromosomes. Primed in situ labeling (PRINS) was used to locate the 180-bp knob DNA sequences on mitotic metaphase chromosomes of several maize lines. The chromosomal regions labeled by PRINS corresponded to the reported C bands found in these lines. Additionally, PRINS was used to identify knob-bearing regions in anaphase spreads of a line carrying the st1 mutant and a nonmutant line having a similar number of chromosome knobs. The increase in abnormal anaphase figures in the st1 mutant was not accompanied by an increase in association of knob DNA with abnormal anaphases. Thus, the increase in chromosomal stickiness appears to be due to an increase in stickiness of knob and nonknob chromosomal regions. The mechanism responsible for the st1 mutant, therefore, is hypothesized to be different from that implicated in the other previously described sticky chromosomes situations.