About this Research Topic
In recent years, several studies have found that morphological changes of organelles also affect the cell cycle. DRP1 depletion causes mitochondrial fission defects and decreases cyclin E expression. Depletion of MFF, recruiter of DRP1 on mitochondria, results in the mis-alignment of mitotic chromosomes. In fact, fragmented mitochondria in mitotic cells associate with spindle microtubes to move towards the end of spindle and this transportation is mediated by the Rho GTPase Miro. Miro also regulates the ER and mitochondria contact sites, where mitochondrial fission happens, and recruits the outer kinetochore protein CENP-F to mitochondria at the time of cytokinesis. Therefore, mitochondrial morphological changes and transportation are tightly linked to mitotic progress.
In this Research Topic, we focus on the crosstalk between subcellular organelles and the mitotic/meiotic spindle and chromosomes. We are particularly interested in understanding how mitotic and meiotic kinases regulate morphological changes of mitochondria/ER/Golgi body and how these morphology changes affect mitotic and meiotic progress at the cellular and molecular level. The ultimate goal is to uncover how morphological changes of organelles and mitotic and meiotic progression are linked.
The specific themes for this Research Topic include, but are not limited to the following:
• Mitotic/meiotic kinases that are essential for the morphological changes of mitochondria/ER/Golgi body and the underlying molecular mechanisms.
• New proteins on mitochondria/ER/Golgi body that can affect mitosis/meiosis
• The signaling pathways affecting both subcellular organelle morphology and mitosis/meiosis
• New strategies of imaging and quantifying cellular morphology changes and spindle formation defects.
• Studies uncovering defects in (sub)cellular organelle morphology changes in disease states.
• Reviews that comprehensively cover the most recent progress within this topic.
Keywords: Mitosis, meiosis, spindle, mitochondria, Golgi body
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