Publications by authors named "R E Karess"

spp. may cause opportunistic infections called vulvovaginal candidiasis (VVC), which is estimated to be the second most common cause of vaginitis worldwide. Under various circumstances, VVC could compromise pregnancy outcomes.

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Drosophila testes are a powerful model system for studying biological processes including stem cell biology, nuclear architecture, meiosis and sperm development. However, immunolabeling of the whole Drosophila testis is often associated with significant non-uniformity of staining due to antibody penetration. Squashed preparations only partially overcome the problem since it decreases the 3D quality of the analyses.

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Article Synopsis
  • The RZZ complex, made up of Rough-Deal (Rod), Zw10, and Zwilch, is crucial for the spindle assembly checkpoint (SAC), which ensures proper separation of sister chromatids during mitosis.
  • Researchers studied the Rod_C domain to see its role in RZZ function by introducing mutations and observed that some mutations hindered RZZ's ability to recruit to kinetochores, even though they could still form a complex with Zw10 and Zwilch.
  • The findings indicate that the Rod_C domain is important for the interactions that allow RZZ to operate effectively at kinetochores.
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The Mad1 spindle checkpoint protein helps organize several nucleoplasmic components, and flies lacking Mad1 present changes in gene expression reflecting altered chromatin conformation. In interphase, checkpoint protein Mad1 is usually described as localizing to the inner nuclear envelope by binding the nucleoporin Tpr, an interaction believed to contribute to proper mitotic regulation. Whether Mad1 has other nuclear interphase functions is unknown.

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Tissue homeostasis requires accurate control of cell proliferation, differentiation and chromosome segregation. Drosophila sas-4 and aurA mutants present brain tumours with extra neuroblasts (NBs), defective mitotic spindle assembly and delayed mitosis due to activation of the spindle assembly checkpoint (SAC). Here we inactivate the SAC in aurA and sas-4 mutants to determine whether the generation of aneuploidy compromises NB proliferation.

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