Adaptive management assists reintroduction as higher tides threaten an endangered salt marsh plant

In theory, extirpated plant species can be reintroduced and managed to restore sustainable populations. However, few reintroduced plants are known to persist for more than a few years. Our adaptive‐management case study illustrates how we restored the endangered hemiparasitic annual plant, Chloropyron maritimum subsp. maritimum (salt marsh bird's beak), to Sweetwater Marsh, San Diego Bay National Wildlife Refuge, California, United States, and used monitoring and experimentation to identify the factors limiting the reintroduced population. After extirpation in 1988, reintroduction starting that year led to a resilient, genetically diverse population in 2016 (a “boom” of approximately 14,000) that rebounded from a “bust” (62 in 2014). Multiple regressions attributed 82% of the variation in population counts to tidal amplitude, rainfall, and temperature. Populations of salt marsh bird's beak crashed when the diurnal tide range peaked during the 18.6‐year lunar nodal cycle (a rarely considered factor that periodically added approximately 12 cm to tidal ranges). We explain booms as follows: During smaller tidal amplitudes, above‐average rainfall could desalinize upper intertidal soils and stimulate salt marsh bird's beak germination. Then, moderate temperature in May favors growth to reproduction in June. In addition, salt marsh bird's beak needs a short and open canopy of native perennial plants, with roots to parasitize (not non‐native annual grass pseudohosts) and nearby upland soil for a preferred pollinator, ground‐burrowing bees. Although our reintroduced salt marsh bird's beak population is an exceptional case of persistence, this rare species‐specific environmental and biological requirement makes it vulnerable to rising sea levels and global warming.     

Identification of the receptor binding domain of the mouse mammary tumor virus envelope protein

Mouse mammary tumor virus (MMTV) is a betaretrovirus that infects rodent cells and uses mouse transferrin receptor 1 for cell entry. To characterize the interaction of MMTV with its receptor, we aligned the MMTV envelope surface (SU) protein with that of Friend murine leukemia virus (F-MLV) and identified a putative receptor-binding domain (RBD) that included a receptor binding sequence (RBS) of five amino acids and a heparin-binding domain (HBD). Mutation of the HBD reduced virus infectivity, and soluble heparan sulfate blocked infection of cells by wild-type pseudovirus. Interestingly, some but not all MMTV-like elements found in primary and cultured human breast cancer cell lines, termed h-MTVs, had sequence alterations in the putative RBS. Single substitution of one of the amino acids found in an h-MTV RBS variant in the RBD of MMTV, Phe(40) to Ser, did not alter species tropism but abolished both virus binding to cells and infectivity. Neutralizing anti-SU monoclonal antibodies also recognized a glutathione S-transferase fusion protein that contained the five-amino-acid RBS region from MMTV. The critical Phe(40) residue is located on a surface of the MMTV RBD model that is distant from and may be structurally more rigid than the region of F-MLV RBD that contains its critical binding site residues. This suggests that, in contrast to other murine retroviruses, binding to its receptor may result in few or no changes in MMTV envelope protein conformation.     

Mutations in Smooth Muscle Alpha-Actin (ACTA2) Cause Coronary Artery Disease, Stroke, and Moyamoya Disease, Along with Thoracic Aortic Disease

The vascular smooth muscle cell (SMC)-specific isoform of α-actin (ACTA2) is a major component of the contractile apparatus in SMCs located throughout the arterial system. Heterozygous ACTA2 mutations cause familial thoracic aortic aneurysms and dissections (TAAD), but only half of mutation carriers have aortic disease. Linkage analysis and association studies of individuals in 20 families with ACTA2 mutations indicate that mutation carriers can have a diversity of vascular diseases, including premature onset of coronary artery disease (CAD) and premature ischemic strokes (including Moyamoya disease [MMD]), as well as previously defined TAAD. Sequencing of DNA from patients with nonfamilial TAAD and from premature-onset CAD patients independently identified ACTA2 mutations in these patients and premature onset strokes in family members with ACTA2 mutations. Vascular pathology and analysis of explanted SMCs and myofibroblasts from patients harboring ACTA2 suggested that increased proliferation of SMCs contributed to occlusive diseases. These results indicate that heterozygous ACTA2 mutations predispose patients to a variety of diffuse and diverse vascular diseases, including TAAD, premature CAD, ischemic strokes, and MMD. These data demonstrate that diffuse vascular diseases resulting from either occluded or enlarged arteries can be caused by mutations in a single gene and have direct implications for clinical management and research on familial vascular diseases.     

The Salmonella typhimurium glycine cleavage enzyme system

Summary A glycine cleavage enzyme system, inducible by glycine, has been demonstrated in Salmonella typhimurium. The induced enzyme levels, however, are only about 20% of the induced levels found in Escherichia coli. Starting with a serine auxotroph, mutants were isolated that grow with a serine supplement, but not with a glycine supplement. Three independently isolated mutants have reduced or nondetectable glycine cleavage enzyme levels. The new mutations, designated gcv, were mapped between the serA and lys genes at 62.5 min on the S. typhimurium chromosome.Abbreviations C1 one-carbon - GCV glycine cleavage - GM glucose minimal - L agar Luria agar - LB Luria broth - Tc tetracycline