Water Chemistry and Lake Dynamics of Laguna Bacalar, Quintana Roo, Mexico

Laguna Bacalar in the Quintana Roo region is the second largest lake in Mexico and contains freshwater derived solely from groundwater. Local geology on the Yucatan Peninsula is karstic and the southern shoreline of Laguna Bacalar is spotted with a handful of cenotes that contribute substantial amounts of inflowing groundwater to the lake. This is shown by sonde profile data taken in one of the largest cenotes in the area. Outflow is dominated by a surface water outlet in the southern portion of the lake and an unknown amount of outflowing groundwater. During January of 2017 through 2019, UWM researchers collected data on the physical flow to and from the lake, δ13C, δ18O and δ2H isotopes, and major ion chemistry in order to provide insight into the overall chemical and physical hydrology of the lake. The primary hydrochemical processes controlling lake chemistry include influx of high alkalinity groundwater in the southern portion, CO2 evolution and a resultant pH rise and calcite precipitation. Saturation indices modeled using PHREEQC indicate the water in Laguna Bacalar is oversaturated with calcite and at saturation with gypsum. The northern portion of the lake has no groundwater influx and is dominated by evaporative effects. Recently, the lake and the city of Bacalar have gained international attention and are attracting an increasing number of visitors. While fueling a growing tourism industry and economy, this raises the potential for accelerating human impacts that can threaten the health of this relatively pristine freshwater ecosystem. Understanding the basic hydrology of Laguna Bacalar will be a key element in managing water quality and preserving the truly unique hydrogeological and biological characteristics of the system

LIN28 lets BLIMP1 Take the Right Course

The transcription factor BLIMP1 is a master regulator of primordial germ cell (PGC) specification and is suppressed by the microRNA let-7. In a recent issue of Nature, West and colleagues use a unique in vitro ES cell differentiation strategy to show that LIN28 is an essential regulator of PGC formation through inhibition of let-7 maturation and consequential induction of BLIMP1

Spermatozoa lacking Fertilization Influencing Membrane Protein (FIMP) fail to fuse with oocytes in mice

Fujihara, Y., Lu, Y., Noda, T., Oji, A., Larasati, T., Kojima-Kita, K., . . . Ikawa, M. (2020). Spermatozoa lacking fertilization influencing membrane protein (FIMP) fail to fuse with oocytes in mice. Proceedings of the National Academy of Sciences of the United States of America, 117(17), 9393-9400. doi:10.1073/pnas.191706011

Loss of inhibin alpha uncouples oocyte-granulosa cell dynamics and disrupts postnatal folliculogenesis

AbstractTargeted disruption of the inhibin α gene (Inha–/–) in mice results in an ovarian phenotype of granulosa cell tumors that renders the animals infertile. Little is known about the reproductive defects prior to tumor development. Here, we report novel data on early follicle dynamics in Inha–/– mice, which demonstrate that inhibin α has important consequences upon follicle development. Morphological changes in both germ and somatic cells were evident in postnatal day 12 ovaries, with Inha−/− mice exhibiting numerous multilayered follicles that were far more advanced than those observed in age-matched controls. These changes were accompanied by alterations in follicle dynamics such that Inha−/− ovaries had fewer follicles in the resting pool and more committed in the growth phase. Absence of inhibin α resulted in advanced follicular maturation as marked by premature loss of anti-Müllerian hormone (AMH) in secondary follicles. Additionally, gene expression analysis revealed changes in factors known to be vital for oocyte and follicle development. Together, these data provide key evidence to suggest that regulation of the inhibin/activin system is essential for early folliculogenesis in the prepubertal mouse ovary

Nine genes abundantly expressed in the epididymis are not essential for male fecundity in mice

Noda, T., Sakurai, N., Nozawa, K., Kobayashi, S., Devlin, D. J., Matzuk, M. M., & Ikawa, M. (2019). Nine genes abundantly expressed in the epididymis are not essential for male fecundity in mice. Andrology, 7(5), 644-653. doi:10.1111/andr.1262

Disruption of Gastrulation and Heparan Sulfate Biosynthesis in EXT1-Deficient Mice

AbstractMutations in the EXT1 gene are responsible for human hereditary multiple exostosis type 1. The Drosophila EXT1 homologue, tout-velu, regulates Hedgehog diffusion and signaling, which play an important role in tissue patterning during both invertebrate and vertebrate development. The EXT1 protein is also required for the biosynthesis of heparan sulfate glycosaminoglycans that bind Hedgehog. In this study, we generated EXT1-deficient mice by gene targeting. EXT1 homozygous mutants fail to gastrulate and generally lack organized mesoderm and extraembryonic tissues, resulting in smaller embryos compared to normal littermates. RT-PCR analysis of markers for visceral endoderm and mesoderm development indicates the delayed and abnormal development of both of these tissues. Immunohistochemical staining revealed a visceral endoderm pattern of Indian hedgehog (Ihh) in wild-type E6.5 embryos. However, in both EXT1-deficient embryos and wild-type embryos treated with heparitinase I, Ihh failed to associate with the cells. The effect of the EXT1 deletion on heparan sulfate formation was tested by HPLC and cellular glycosyltransferase activity assays. Heparan sulfate synthesis was abolished in EXT1 −/− ES cells and decreased to less than 50% in +/− cell lines. These results indicate that EXT1 is essential for both gastrulation and heparan sulfate biosynthesis in early embryonic development

Sperm proteins SOF1, TMEM95, and SPACA6 are required for sperm-oocyte fusion in mice

Noda, T., Lu, Y., Fujihara, Y., Oura, S., Koyano, T., Kobayashi, S., . . . Ikawa, M. (2020). Sperm proteins SOF1, TMEM95, and SPACA6 are required for sperm-oocyte fusion in mice. Proceedings of the National Academy of Sciences of the United States of America, 117(21) doi:10.1073/pnas.192265011

Genetic evidence that SMAD2 is not required for gonadal tumor development in inhibin-deficient mice

<p>Abstract</p> <p>Background</p> <p>Inhibin is a tumor-suppressor and activin antagonist. Inhibin-deficient mice develop gonadal tumors and a cachexia wasting syndrome due to enhanced activin signaling. Because activins signal through SMAD2 and SMAD3 in vitro and loss of SMAD3 attenuates ovarian tumor development in inhibin-deficient females, we sought to determine the role of SMAD2 in the development of ovarian tumors originating from the granulosa cell lineage.</p> <p>Methods</p> <p>Using an inhibin α null mouse model and a conditional knockout strategy, double conditional knockout mice of Smad2 and inhibin alpha were generated in the current study. The survival rate and development of gonadal tumors and the accompanying cachexia wasting syndrome were monitored.</p> <p>Results</p> <p>Nearly identical to the controls, the Smad2 and inhibin alpha double knockout mice succumbed to weight loss, aggressive tumor progression, and death. Furthermore, elevated activin levels and activin-induced pathologies in the liver and stomach characteristic of inhibin deficiency were also observed in these mice. Our results indicate that SMAD2 ablation does not protect inhibin-deficient females from the development of ovarian tumors or the cachexia wasting syndrome.</p> <p>Conclusions</p> <p>SMAD2 is not required for mediating tumorigenic signals of activin in ovarian tumor development caused by loss of inhibin.</p