Biology subjects

Biton, I.

Publications and source records attributed to Biton, I..

3 recordsLinked to original sources

bioRxiv2026

β-Carbonic anhydrase SlβCA4 is required for normal growth, carbon assimilation and stomatal plasticity in tomato

{beta}-Carbonic anhydrases ({beta}CAs) catalyze the reversible interconversion of CO2 and bicarbonate and contribute to plant carbon metabolism and environmental responses. However, the physiological functions of individual {beta}CA isoforms in crops remain poorly understood. Here, we investigated two chloroplast-localized {beta}CAs, Sl{beta}CA1 and Sl{beta}CA4, in tomato (Solanum lycopersicum). We combined subcellular localization, CRISPR/Cas9 mutagenesis, grafting, leaf gas-exchange measurements, and controlled environmental treatments to examine their roles in growth, photosynthesis, and stomatal developmental plasticity. Both proteins localized to chloroplasts but their disruption resulted in markedly different phenotypes. While Sl{beta}CA1 mutants showed largely normal growth and photosynthesis, Sl{beta}CA4 mutants exhibited severe root and shoot growth defects. Grafting mutant shoots onto wild-type rootstocks partially restored vegetative growth, indicating that impaired root function contributes to the growth defects. Sl{beta}CA4 mutants also showed reduced CO2 assimilation and stomatal conductance, while electron transport remained largely unaffected. Elevated CO2 partially improved leaflet growth but did not restore plant height or root elongation. Furthermore, unlike wild-type plants, Sl{beta}CA4 mutants failed to increase stomatal index in response to elevated temperature. These findings reveal distinct physiological roles for chloroplast-localized {beta}CAs in tomato and identify Sl{beta}CA4 as an important contributor to plant growth, photosynthesis, and temperature-dependent stomatal developmental plasticity.

plant biology↗

bioRxiv2022

Store-operated Ca2+ entry regulatory factor (SARAF) alters murine metabolic state in an age-dependent manner via hypothalamic pathways.

Store-operated Ca2+ entry (SOCE) is a vital process aimed at refilling cellular internal Ca2+ stores, and a primary cellular-signaling driver of transcription factors entry to the nucleus. SARAF (SOCE associated regulatory factor)/TMEM66 is an endoplasmic reticulum (ER) resident transmembrane protein that promotes SOCE inactivation and prevents Ca2+ overfilling of the cell. Here we demonstrate that mice deficient in SARAF develop age-dependent sarcopenic obesity with decreased energy expenditure, lean mass and locomotion without affecting food consumption. Moreover, SARAF ablation reduces hippocampal proliferation, modulates the activity of the hypothalamus-pituitary-adrenal (HPA) axis, and mediates changes in anxiety-related behaviors. Interestingly, selective SARAF ablation in the paraventricular nucleus (PVN) of the hypothalamus protects from old age-induced obesity and preserves locomotion, lean mass and energy expenditure, suggesting an opposing, site-specific role for SARAF. Lastly, SARAF ablation in hepatocytes leads to elevated SOCE, elevated vasopressin-induced Ca2+ oscillations, and an increased mitochondrial spare respiratory capacity, thus providing insights into the cellular mechanisms that may affect the global phenotypes. These effects may be mediated via the liver X receptor (LXR) and IL-1 signaling metabolic regulators explicitly altered in SARAF ablated cells. In short, our work supports both central and peripheral roles of SARAF in regulating metabolic, behavioral, and cellular responses. HighlightsO_LILoss/absence of SARAF facilitates age-dependent obesity with decreased metabolic rate, lean mass, and locomotion, without affecting food consumption. C_LIO_LILoss of SARAF leads to lipid droplet hypertrophy, BAT whitening and age-dependent hepatic steatosis. C_LIO_LIMice lacking SARAF expression in the PVN have an increased metabolic rate, decreased BAT whitening, and are protected from sarcopenic obesity. C_LIO_LISARAF ablation in hepatocytes increases SOCE, elevates Ca2+ oscillation in response to vasopressin, and increases the mitochondrias spare respiratory capacity. C_LIO_LILoss of SARAF leads to decreased hippocampal proliferation, sensitized HPA-axis and changes in anxiety-related behavior. C_LI

physiology↗

bioRxiv2019

Regulation of CHD2 expression by the Chaserr long noncoding RNA is essential for viability

Genomic loci adjacent to genes encoding for transcription factors and chromatin remodelers are enriched for long non-coding RNAs (lncRNAs), but the functional importance of this enrichment is largely unclear. Chromodomain helicase DNA binding protein 2 (Chd2) is a chromatin remodeller with various reported functions in cell differentiation and DNA damage response. Heterozygous mutations in human CHD2 have been implicated in epilepsy, neurodevelopmental delay, and intellectual disability. Here we show that Chaserr, a highly conserved lncRNA transcribed from a region near the transcription start site of Chd2 and on the same strand, acts in concert with the CHD2 protein to maintain proper Chd2 expression levels. Loss of Chaserr in mice leads to early postnatal lethality in homozygous mice, and severe growth retardation in heterozygotes. Mechanistically, loss of Chaserr leads to substantially increased Chd2 mRNA and protein levels, which in turn lead to increased transcriptional interference by inhibiting promoters found downstream of highly expressed genes. We further show that Chaserr production represses Chd2 expression solely in cis, and that the phenotypic consequences of Chaserr loss are rescued when Chd2 is perturbed as well. Targeting Chaserr is thus a potentially viable strategy for increasing CHD2 levels in haploinsufficient individuals.

molecular biology↗