Cambrian radiation speciation events driven by sea level and redoxcline changes on the Siberian Craton.

The evolutionary processes of speciation during the Cambrian radiation and their potential extrinsic drivers, such as episodic oceanic oxygenation events, remain unconfirmed. High-resolution temporal and spatial distribution of reef-associated archaeocyath sponge species on the Siberian Craton during the early Cambrian [ca. 528 to 510 million years ago] shows that speciation was driven by increased endemism particularly ca. 521 million years (59.7% endemic species) and 514.5 million years (65.25% endemic species) ago. These mark rapid speciation events after dispersal of ancestors from the Aldan-Lena center of origin to other regions. These speciation events coincided with major sea-level lowstands, which we hypothesize were intervals when relative deepening of the shallow redoxcline permitted extensive oxygenation of shallow waters over the entire craton. This provided oxic corridors for dispersal and allowed the formation of new founder communities. Thus, shallow marine oxygen expansion driven by sea-level oscillations provides an evolutionary driver for sucessive speciation events during the Cambrian radiation.

Conflicting evidence for the role of JNK as a target in breast cancer cell proliferation: Comparisons between pharmacological inhibition and selective shRNA knockdown approaches.

As a target, the JNK pathway has been implicated in roles including cell death, proliferation, and inflammation in variety of contexts which span cardiovascular disease, neurodegenerative pathologies, and cancer. JNK1 and JNK2 have recently been demonstrated to function independently, highlighting a new parameter in the study of the JNK pathway. In order for JNK1 and JNK2-specific roles to be defined, better tools need to be employed. Previous studies have relied upon the broad spectrum JNK inhibitor, SP600125, to characterize the role of JNK signaling in a number of cell lines, including the breast cancer cell line MCF-7. In line with previous literature, our study has demonstrated that SP600125 treatment inhibited c-Jun and JNK phosphorylation and MCF-7 proliferation. However, in addition to targeting JNK1, JNK2, and JNK3, SP600125 has been previously demonstrated to suppress the activity of a number of other serine/threonine kinases, making SP600125 an inadequate tool for JNK isoform-specific roles to be determined. In this study, lentiviral shRNA was employed to selectively knockdown JNK1, JNK2, and JNK1/2 in MCF-7 cells. Using this approach, JNK phosphorylation was fully inhibited following stable knockdown of respective JNK isoforms. Interestingly, despite suppression of JNK phosphorylation, MCF-7 cell proliferation, cell cycle progression, or cell death remained unaffected. These findings raise the question of whether JNK phosphorylation really is pivotal in MCF-7 cell growth and death or if suppression of these events is a result of one of the many off-targets cited for SP600125.