Population genetics,demographic and evolutionary history of the Dudley’s lousewort (Pedicularis dudleyi), a rare redwood forest specialist

Pedicularis dudleyi (Dudley’s Lousewort, Orobanchaceae) is an extremely rare plant endemic to the redwood forests of Central California. Until recently, the species was known only from three extant natural populations. However, in 2019, one of those populations was described as a novel species (P. rigginsiae D.J. Keil) based on morphological and ecological data leaving only two populations described as P. dudleyi. While little is known about the past distribution of the species, historical records have led to speculation that the species was once more widespread and may have suffered from habitat destruction as a result of widespread logging during the early twentieth century. We utilized a combination of ddRAD SNP and Sanger sequencing data to: (1) Test the morphological hypothesis that P. rigginsiae is distinct from P. dudleyi; (2) Describe the genetic diversity and population structure of P. dudleyi and; (3) Test the hypothesis that the species underwent a bottleneck corresponding with increased logging of redwood forests in the early twentieth century. Our results support the recognition of P. rigginsiae as distinct from P. dudleyi, increasing the conservation priority of both species. Genetic diversity statistics and analyses of genetic structure suggest that both populations of P. dudleyi are highly differentiated from each other with one population exhibiting unexpected substructure. Finally, demographic modeling supports a scenario where the contemporary rarity of the species is explained by a recent bottleneck.

     

Agricultural Landscape Transformation Needed to Meet Water Quality Goals in the Yahara River Watershed of Southern Wisconsin

Ecosystems - Balancing agricultural production with other ecosystem services is a vexing challenge. The Yahara River watershed in southern Wisconsin is a place where tensions among farmers,...     

Potential Facilitation Between a Commensal and a Pathogenic Microbe in a Wildlife Disease

We assessed the potential for microbial interactions influencing a well-documented host–pathogen system. Mycoplasma agassizii is the known etiological agent of upper respiratory tract disease in Mojave desert tortoises (Gopherus agassizii), but disease in wild animals is extremely heterogeneous. For example, a much larger proportion of animals harbor M. agassizii than those that develop disease. With the availability of a new quantitative PCR assay for a microbe that had previously been implicated in disease, Pasteurella testudinis, we tested 389 previously collected samples of nasal microbes from tortoise populations across the Mojave desert. We showed that P. testudinis is a common commensal microbe. However, we did find that its presence was associated with higher levels of M. agassizii among the tortoises positive for this pathogen. The best predictor of P. testudinis prevalence in tortoise populations was average size of tortoises, suggesting that older populations have higher levels of P. testudinis. The prevalence of co-infection in populations was associated with the prevalence of URTD, providing additional evidence for an indirect interaction between the two microbes and inflammatory disease. We showed that URTD, like many chronic, polymicrobial diseases involving mucosal surfaces, shows patterns of a polymicrobial etiology.

     

Body size changes in bivalves of the family Limidae in the aftermath of the end‐Triassic mass extinction: the Brobdingnag effect

Reduction in body size of organisms following mass extinctions is well‐known and often ascribed to the Lilliput effect. This phenomenon is expressed as a temporary body size reduction within surviving species. Despite its wide usage the term is often loosely applied to any small post‐extinction taxa. Here we assess the size of bivalves of the family Limidae (Rafineque) prior to, and in the aftermath of, the end‐Triassic mass extinction event. Of the species studied only one occurs prior to the extinction event, though is too scarce to test for the Lilliput effect. Instead, newly evolved species originate at small body sizes and undergo a within‐species size increase, most dramatically demonstrated by Plagiostoma giganteum (Sowerby) which, over two million years, increases in size by 179%. This trend is seen in both field and museum collections. We term this within‐species size increase of newly originated species in the aftermath of mass extinction, the Brobdingnag effect, after the giants that were contemporary with the Lilliputians in Swift's Gulliver's Travels. The size increase results from greater longevity and faster growth rates. The cause of the effect is unclear, although it probably relates to improved environmental conditions. Oxygen‐poor conditions in the Early Jurassic are associated with populations of smaller body size caused by elevated juvenile mortality but these are local/regional effects that do not alter the long‐term, size increase. Although temperature‐size relationships exist for many organisms (Temperature‐Size Rule and Bergmann's Rule), the importance of this is unclear here because of a poorly known Early Jurassic temperature record.     

Mycobacterium tuberculosis encodes a YhhN family membrane protein with lysoplasmalogenase activity that protects against toxic host lysolipids

The pathogen Mycobacterium tuberculosis (M.tb) resides in human macrophages, wherein it exploits host lipids for survival. However, little is known about the interaction between M.tb and macrophage plasmalogens, a subclass of glycerophospholipids with a vinyl ether bond at the sn-1 position of the glycerol backbone. Lysoplasmalogens, produced from plasmalogens by hydrolysis at the sn-2 carbon by phospholipase A₂, are potentially toxic but can be broken down by host lysoplasmalogenase, an integral membrane protein of the YhhN family that hydrolyzes the vinyl ether bond to release a fatty aldehyde and glycerophospho-ethanolamine or glycerophospho-choline. Curiously, M.tb encodes its own YhhN protein (MtbYhhN), despite having no endogenous plasmalogens. To understand the purpose of this protein, the gene for MtbYhhN (Rv1401) was cloned and expressed in Mycobacterium smegmatis (M.smeg). We found the partially purified protein exhibited abundant lysoplasmalogenase activity specific for lysoplasmenylethanolamine or lysoplasmenylcholine (pLPC) (V_max∼15.5 μmol/min/mg; K_m∼83 μM). Based on cell density, we determined that lysoplasmenylethanolamine, pLPC, lysophosphatidylcholine, and lysophosphatidylethanolamine were not toxic to M.smeg cells, but pLPC and LPC were highly toxic to M.smeg spheroplasts, which are cell wall–deficient mycobacterial forms. Importantly, spheroplasts prepared from M.smeg cells overexpressing MtbYhhN were protected from membrane disruption/lysis by pLPC, which was rapidly depleted from the media. Finally, we found that overexpression of full-length MtbYhhN in M.smeg increased its survival within human macrophages by 2.6-fold compared to vector controls. These data support the hypothesis that MtbYhhN protein confers a growth advantage for mycobacteria in macrophages by cleaving toxic host pLPC into potentially energy-producing products.     

Flow cytometric method for quantifying viable Mycoplasma agassizii,an agent of upper respiratory tract disease in the desert tortoise (Gopherus agassizii)

Aims: Mycoplasma agassizii can cause upper respiratory tract disease in the threatened desert tortoise of the Southwestern United States. Two technical challenges have impeded critical microbiological studies of this microorganism: (i) its small size limits the use of light microscopy for cell counting and (ii) its extremely slow growth in broth and agar cultures impedes colony counting. Our aim was to develop a rapid and sensitive flow cytometric method using a vital fluorescent dye to enumerate viable M. agassizii cells. Methods and Results: Here, we demonstrate that the nonfluorescent molecule 5‐carboxyfluorescein (5‐CF) diacetate acetoxymethyl ester penetrates M. agassizii cell membranes and it is converted in the cytoplasm to the fluorescent molecule 5‐CF by the action of intracellular esterases. Labelled mycoplasma cells can be easily detected by flow cytometry, and cultures with as few as 100 viable mycoplasma cells ml^?1 can be labelled and counted in less than 1 h. Experiments using temperature‐induced cell death demonstrated that only viable M. agassizii cells are labelled with this procedure. Conclusions: A rapid and sensitive flow cytometric technique has been developed for enumerating viable M. agassizii cells. Significance and Impact of the Study: This technique should facilitate basic immunological, biochemical and pharmacological studies of this important pathogen which may lead to new diagnostic and therapeutic methods.     

The mitotic centromeric protein MEI-S332 and its role in sister-chromatid cohesion

Faithful segregation of sister chromatids during cell division requires properly regulated cohesion between the sister centromeres. The sister chromatids are attached along their lengths, but particularly tightly in the centromeric regions. Therefore specific cohesion proteins may be needed at the centromere. Here we show that Drosophila MEI-S332 protein localizes to mitotic metaphase centromeres. Both overexpression and mutation of MEI-S332 increase the number of apoptotic cells. In mei-S332 mutants the ratio of metaphase to anaphase figures is lower than wild type, but it is higher if MEI-S332 is overexpressed. In chromosomal squashes centromeric attachments appear weaker in mei-S332 mutants than wild type and tighter when MEI-S332 is overexpressed. These results are consistent with MEI-S332 contributing to centromeric sister-chromatid cohesion in a dose-dependent manner. MEI-S332 is the first member identified of a predicted class of centromeric proteins that maintain centromeric cohesion. Received: 11 December 1998; in revised form: 4 August 1999 / Accepted: 13 August 1999