Specifically, Aurora B localizes to the chromosomes in prophase, the centromere in prometaphase and metaphase, and the central mitotic spindle in anaphase.

Finally, a portion of the tagged Aurora B localized to the equatorial cell cortex, having been transported to this location by astral microtubules.

In topoisomerase II-depleted cells, Aurora B and INCENP do not transfer to the central spindle in late mitosis.

Also, cells deficient in topoisomerase II show significantly reduced Aurora B kinase activity.

Studies in several organisms indicate that Aurora B oversees chromosome biorientation by ensuring that appropriate connections are made between spindle microtubules and kinetochores.

Inhibition of Aurora B function by RNA interference[16] or microinjection of blocking antibodies[17] impairs the alignment of chromosomes at the equator of the mitotic spindle.

Numerous kinetochore targets of Aurora kinases have been determined in organisms ranging from yeast to man.

Importantly, inhibition of MCAK by a number of approaches leads to improper attachment of kinetochores to spindle microtubules.

[21] It has been hypothesized that tension generated by amphitelic attachment (biorientation; the attachment of sister kinetochores to opposite spindle poles) pulls sister kinetochores apart, thus disrupting the interaction of Aurora B at the innermost portion of the centromere with microtubule binding sites on the fibrous corona of the outermost centromere.

[24] However, in Xenopus egg cell-free extracts, condensin binding and chromosome condensation occur normally even in the absence of Aurora B.

Aurora B localizes to the paired arms of homologous chromosomes in metaphase I of C. elegans meiosis, and perturbs microtubule dynamics in mitosis.

[27] In mitotic vertebrate B lymphocytes, the proper centromeric localization of a number of Aurora B binding partners requires cohesin.

Inhibition of Aurora B activity prevents proper myosin II localization to the cleavage furrow and disrupts spindle midzone organization.

[32] The spindle assembly checkpoint inhibits progression of mitosis from metaphase to anaphase until all sister chromatid pairs are bioriented.

[33][34] Aurora B may be involved in the localization of MAD2 and BubR1, proteins that recognize correct chromosome attachment to spindle microtubules.

Following axotomy of cultured neurons, significant upregulation in Aurora B kinase gene expression was observed coinciding with regenerative axonal sprouting.

[46] Furthermore, overexpression of Aurora B kinase results in accelerated axonal outgrowth of spinal motor neurons in developing zebrafish.