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Serpentinites and serpentinized mantle peridotites with various tectonic origins occur in the Franciscan Complex of the Northern California Cordillera, USA. Boron isotopes of serpentinites differentiate with fluid-mediated processes, and have great potential for key geologic markers in convergent margins. To understand boron isotope behavior within the Franciscan subduction zone system, we apply a newly developed ablation volume correction (AVC) method for in-situ isotope/elemental analyses using a laser-ablation multiple collector inductively-coupled-plasma mass spectrometry (LA-MC-ICPMS) on seventeen different Franciscan serpentinites (sensu lato) collected from eight separate areas. Boron abundances and isotope compositions of the studied serpentinites show large variations B = 1.6–239 μg·g−1, δ11B = −12.0 to +24.4‰, which allow to discriminate the serpentinites into two groups: (1) a lighter δ11B of −12.0 to +8.8‰ with a lesser B ~2 GPa. Preferential partitioning of 11B into fluids released from the subducted slab at shallow leaves lighter δ11B in the slab resulting in lighter δ11B in the deep slab fluids. In contrast, the blueschist-absent serpentinites with heavier δ11B may have formed at a shallow environment where shallow slab or hydrothermal fluids with heavier 11B were present. Lesser versus greater amounts of B in the deep versus shallow serpentinites are also consistent with the dehydration profile of B from a slab. Our results show the versatility of boron isotopes and composition for identification of the origin of serpentinite in Pacific-type orogenic belts.

Neuron-restrictive silencer factor (NRSF) is a zinc-finger transcription factor that binds to specific DNA sequences (NRSE) to repress transcription. By down-regulating the transcription of its target genes, NRSF contributes to the regulation of various biological processes, including neuronal differentiation, carcinogenesis and cardiovascular homeostasis. We previously reported that NRSF regulates expression of the cardiac fetal gene program, and that attenuation of NRSF-mediated repression contributes to genetic remodeling in hearts under pathological conditions. The precise molecular mechanisms and signaling pathways via which NRSF activity is regulated in pathological conditions of the heart remain unclear, however. In this study, to search for regulators of NRSF, we carried out yeast two-hybrid screening using NRSF as bait and identified zinc-finger protein (Zfp) 90 as a novel NRSF-binding protein. NRSF and Zfp90 colocalized in the nucleus, with the zinc-finger DNA-binding domain of the former specifically interacting with the latter. Zfp90 inhibited the repressor activity of NRSF by inhibiting its binding to DNA, thereby derepressing transcription of NRSF-target genes. Knockdown of Zfp90 by siRNA led to reduced expression of NRSF-target fetal cardiac genes, atrial and brain natriuretic peptide genes, and conversely, overexpression of Zfp90 in ventricular myocardium resulted in significant increases in the expression of these genes. Notably, expression of Zfp90 mRNA was significantly upregulated in mouse and human hearts with chronic heart failure. Collectively, these results suggest that Zfp90 functions as a negative regulator of NRSF and contributes to genetic remodeling during the development of cardiac dysfunction.