Intracellular and Extracellular pH and Ca Are Bound to Control Mitosis in the Early Sea Urchin Embryo via ERK and MPF Activities

Abstract

Studies aiming to predict the impact on marine life of ocean acidification and of altered salinity have shown altered development in various species including sea urchins. We have analyzed how external Na, Ca, pH and bicarbonate control the first mitotic divisions of sea urchin embryos. Intracellular free Ca (Cai) and pH (pHi) and the activities of the MAP kinase ERK and of MPF regulate mitosis in various types of cells including oocytes and early embryos. We found that intracellular acidification of fertilized eggs by Na-acetate induces a huge activation of ERK at time of mitosis. This also stops the cell cycle and leads to cell death, which can be bypassed by treatment with the MEK inhibitor U0126. Similar intracellular acidification induced in external medium containing low sodium or 5-(N-Methyl-N-isobutyl) amiloride, an inhibitor of the Na+/H+ exchanger, also stops the cell cycle and leads to cell death. In that case, an increase in Cai and in the phosphorylation of tyr-cdc2 occurs during mitosis, modifications that depend on external Ca. Our results indicate that the levels of pHi and Cai determine accurate levels of Ptyr-Cdc2 and P-ERK capable of ensuring progression through the first mitotic cycles. These intracellular parameters rely on external Ca, Na and bicarbonate, alterations of which during climate changes could act synergistically to perturb the early marine life.

Drosophila ClC‐a is required in glia of the stem cell niche for proper neurogenesis and wiring of neural circuits

“…Thus, it may be that the lack of ClC-a in cortex glia leads to a more acidic extracellular pH due to deficient Cl − recycling for HCO 3 − /Cl − exchangers. Since changes in extracellular and intracellular pH have been shown to affect the proliferative capacity of both wild type and cancer cells (Carswell & Papoutsakis, 2000;Ciapa & Philippe, 2013;Flinck, Kramer, & Pedersen, 2018;Persi et al, 2018;White, Grillo-Hill, & Barber, 2017), ClC-a function in pH regulation could explain the proliferation defects observed in the mutant.…”

Short-chain fatty acids and acidic pH upregulate UT-B, GPR41, and GPR4 in rumen epithelial cells of goats

“…It is well-established that, in epithelial cells (60), endothelial cells (11), bone cells (5), and embryo cells (13), extracellular acidification triggers physiological responses, namely alterations in cell growth (5, 13) and regulation of protein synthesis (11,37,60), under conditions of metabolic acidosis (60) and acute acid loading (11). In the bovine caecum, luminal acidification stimulates monocarboxylate transporter MCT1, a protein which mediates acetate absorption to the serosal side, when the pH on the mucosal side is lowered from 7.4 to 5.5 (28).…”

“…Receptor and ligand levels are sensitively modulated by a variety of microenvironmental changes as well (13,56). Acidity activates GPR4 and evokes expression of a wide range of genes in endothelial cells (11).…”

Resilience of invasive tubeworm (Hydroides dirampha) to warming and salinity stress and its implications for biofouling community dynamics

“…The molecular and/or physiological mechanisms through which reduced salinity halts cleavage and subsequent development warrants further research. Based on observations of other model organisms, some possibilities include reduction of self-assembling ability of the mitotic spindles due to osmotic pressure change, failure of proteins associated with microtubule to function (Sharp 2002), and/or reduction mitosis promoting factor and extracellular regulated kinase activities due to low extracellular sodium ion concentration (Sharp et al 2000;Ciapa and Philippe 2013).…”