The ongoing global pandemic of COVID-19 disease, which is caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), mainly infect lung epithelial cells, and spread mainly through respiratory droplets. However, recent studies showed potential intestinal infection of SARS-CoV-2, implicated the possibility that the intestinal infection of SARS-CoV-2 may correlate with the dysbiosis of gut microbiota, as well as the severity of COVID-19 symptoms. Here, we investigated the alteration of the gut microbiota in COVID-19 patients, as well as analyzed the correlation between the altered microbes and the levels of intestinal inflammatory cytokine IL-18, which was reported to be elevated in the serum of in COVID-19 patients. Comparing with healthy controls or seasonal flu patients, the gut microbiota showed significantly reduced diversity, with increased opportunistic pathogens in COVID-19 patients. Also, IL-18 level was higher in the fecal samples of COVID-19 patients than in those of either healthy controls or seasonal flu patients. Moreover, the IL-18 levels were even higher in the fecal supernatants obtained from COVID-19 patients that tested positive for SARS-CoV-2 RNA than those that tested negative in fecal samples. These results indicate that changes in gut microbiota composition might contribute to SARS-CoV-2-induced production of inflammatory cytokines in the intestine and potentially also to the onset of a cytokine storm.

Background: KMN (KNL/MIS12/NDC80) is a kinetochore constituent essential for chromosome movements in mitosis. Results: KMN protein specifies the kinetochore localization of SKAP. SKAP regulates spindle microtubule dynamics for accurate chromosome movements. Conclusion: The MIS13-SKAP interaction links kinetochore structural components to dynamic microtubule plus-ends. Significance: MIS13-SKAP interaction governs chromosome dynamics and stability in mitosis.

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Background: IQGAP1 is a scaffold protein essential for cellular signaling in response to external cues. Results: Perturbation of the IQGAP1-SKAP interaction results in inhibition of directional cell migration. Conclusion: The IQGAP1-SKAP interaction links to dynamic microtubules at the leading edge to steer cell migration. Significance: IQGAP1 serves as a signaling hub for dynamic interaction between microtubule plus-ends and the cell cortex.