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Gama, V.

Publications and source records attributed to Gama, V..

2 recordsLinked to original sources

Precise tuning of cortical contractility regulates cell shape during cytokinesis

The mechanical properties of the cellular cortex regulate shape changes during cell division, cell migration and tissue morphogenesis. During cell division, contractile force generated by the molecular motor myosin II (MII) at the equatorial cortex drives cleavage furrow ingression. Cleavage furrow ingression in turn increases stresses at the polar cortex, where contractility must be regulated to maintain cell shape during cytokinesis. How polar cortex contractility controls cell shape is poorly understood. We show a balance between MII paralogs allows a fine-tuning of cortex tension at the polar cortex to maintain cell shape during cytokinesis, with MIIA driving cleavage furrow ingression and bleb formation, and MIIB serving as a stabilizing motor and mediating completion of cytokinesis. As the majority of non-muscle contractile systems are cortical, this tuning mechanism will likely be applicable to numerous processes driven by MII contractility.

cell biology

Sox6: A new modulator of renin expression during physiological conditions

Juxtaglomerular (JG) cells, major sources of renin, differentiate from metanephric mesenchymal cells which give rise to JG cells or a subset of smooth muscle cells of the renal afferent arteriole. During periods of dehydration and salt deprivation JG cells undergo expansion. Gene expression profiling comparing resident renal Mesenchymal Stromal Cells (MSCs) with JG cells indicate that the transcription factor Sox6 is highly expressed in JG cells in the adult kidney. In vitro, loss of Sox6 expression reduces differentiation of renal MSCs to renin producing cells. In vivo, Sox6 expression is up-regulated during JG cell expansion. Importantly, knockout of Sox6 in Ren1d+ cells halts the increase in renin expressing cells normally seen during JG cell expansion as well as the typical increase in renin. These results support a previously undefined role for Sox6 in renin expression during normal and pathophysiological conditions.

physiology