SignificanceIn this very large-scale longitudinal field study of the maize rhizosphere microbiome, we identify heritable taxa. These taxa display variance in their relative abundances that can be partially explained by genetic differences between the maize lines, above and beyond the strong influences of field, plant age, and weather on the diversity of the rhizosphere microbiome. If these heritable taxa are associated with beneficial traits, they may serve as phenotypes in future breeding endeavors.

Exocytosis in mammalian spermatozoa (the acrosome reaction) is a process essential for fertilization. Both progesterone and zona pellucida induce exocytosis in spermatozoa, which may encounter both during penetration of the oocyte's vestments. When mouse spermatozoa were exposed first to progesterone and then to zona pellucida, exocytosis was enhanced to a greater degree than that seen when the agonists were presented together or in the inverse order, which suggests that the steroid exerts a priming effect. Progesterone similarly primed the generation of intracellular messengers evoked by zona pellucida. The effects triggered by progesterone were mimicked by gamma-aminobutyric acid (GABA) and were blocked by bicuculline, which indicates that the steroid acts on a GABAA receptor.

In the journey from the male to female reproductive tract, mammalian sperm experience a natural osmotic decrease (e.g., in mouse, from ~415 mOsm in the cauda epididymis to ~310 mOsm in the uterine cavity). Sperm have evolved to utilize this hypotonic exposure for motility activation, meanwhile efficiently silence the negative impact of hypotonic cell swelling. Previous physiological and pharmacological studies have shown that ion channel-controlled water influx/efflux is actively involved in the process of sperm volume regulation; however, no specific sperm proteins have been found responsible for this rapid osmoadaptation. Here, we report that aquaporin3 (AQP3) is a sperm water channel in mice and humans. Aqp3-deficient sperm show normal motility activation in response to hypotonicity but display increased vulnerability to hypotonic cell swelling, characterized by increased tail bending after entering uterus. The sperm defect is a result of impaired sperm volume regulation and progressive cell swelling in response to physiological hypotonic stress during male-female reproductive tract transition. Time-lapse imaging revealed that the cell volume expansion begins at cytoplasmic droplet, forcing the tail to angulate and form a hairpin-like structure due to mechanical membrane stretch. The tail deformation hampered sperm migration into oviduct, resulting in impaired fertilization and reduced male fertility. These data suggest AQP3 as an essential membrane pathway for sperm regulatory volume decrease (RVD) that balances the "trade-off" between sperm motility and cell swelling upon physiological hypotonicity, thereby optimizing postcopulatory sperm behavior.

The gut microbiome harbors a 'silent reservoir' of antibiotic resistance (AR) genes that is thought to contribute to the emergence of multidrug-resistant pathogens through horizontal gene transfer (HGT). To counteract the spread of AR, it is paramount to know which organisms harbor mobile AR genes and which organisms engage in HGT. Despite methods that characterize the overall abundance of AR genes in the gut, technological limitations of short-read sequencing have precluded linking bacterial taxa to specific mobile genetic elements (MGEs) encoding AR genes. Here, we apply Hi-C, a high-throughput, cultureindependent method, to surveil the bacterial carriage of MGEs. We compare two healthy individuals with seven neutropenic patients undergoing hematopoietic stem cell transplantation, who receive multiple courses of antibiotics, and are acutely vulnerable to the threat of multidrug-resistant infections. We find distinct networks of HGT across individuals, though AR and mobile genes are associated with more diverse taxa within the neutropenic patients than the healthy subjects. Our data further suggest that HGT occurs frequently over a several-week period in both cohorts. Whereas most efforts to understand the spread of AR genes have focused on pathogenic species, our findings shed light on the role of the human gut microbiome in this process.

We have investigated whether progesterone-triggered acrosomal exocytosis involves the activation of a gamma-aminobutyric acid (GABA) receptor, and whether activation of this receptor is linked to Ca2+ entry via Ca2+ channels. Mouse spermatozoa preincubated in a modified Tyrode's medium underwent exocytosis when stimulated with progesterone, as revealed by an increase in the number of cells exhibiting an "AR" pattern after staining with chlortetracycline; the effect was concentration dependent. Only capacitated spermatozoa underwent exocytosis in response to progesterone: cells preincubated for 15 min (uncapacitated) did not exocytose in response to this agonist, whereas cells preincubated for 120 min did. Stimulation of capacitated spermatozoa with GABA or muscimol, two GABAA receptor agonists, resulted in acrosomal exocytosis; this response was enhanced by half-maximal concentrations of progesterone. Bicuculline, a GABAA receptor antagonist, inhibited exocytosis stimulated by progesterone or GABA. Picrotoxin, another GABAA receptor antagonist, inhibited only GABA-stimulated exocytosis. These results suggest that progesterone effects are mediated by a GABAA receptor but that such receptor may not be identical to the neuronal GABAA receptor. The ability of progesterone, GABA, or muscimol to stimulate exocytosis was blocked by the Ca2+ channel antagonists verapamil or nifedipine. The Ca2+ channel agonist Bay K 8644, on the other hand, stimulated exocytosis in capacitated sperm cells. The stimulatory ability of progesterone and Bay K 8644 was additive. These results indicate that acrosomal exocytosis involves activation of a GABAA receptor apparently linked to Ca2+ channels.