The polar expression of ENSO and sea-ice variability as recorded in a South Pole ice core

An annually dated ice core recovered from South Pole (2850 m a.s.l.) in 1995, that covers the period 1487–1992, was analyzed for the marine biogenic sulfur species methanesulfonate (MS). Empirical orthogonal function analysis is used to calibrate the high-resolution MS series with associated environmental series for the period of overlap (1973–92). Utilizing this calibration we present a ~500 year long proxy record of the polar expression of the El Niño–Southern Oscillation (ENSO) and southeastern Pacific sea-ice extent variations. These records reveal short-term periods of increased (1800–50, 1900–40) and decreased sea-ice extent (1550–1610, 1660–1710, 1760–1800). In general, increased (decreased) sea-ice extent is associated with a higher (lower) frequency of El Niño events

Hybridization of invasive \u3ci\u3ePhragmites australis\u3c/i\u3e with a native subspecies in North America

Interspecific hybridization can lead to the extinction of native populations and increased aggressiveness in hybrid forms relative to their parental lineages. However, interbreeding among subspecies is less often recognized as a serious threat to native species. Phragmites australis offers an excellent opportunity to investigate intraspecific hybridization since both native and introduced lineages occur in North America. Introduced Phragmites is a highly successful estuarine plant invader throughout North America, but native Phragmites populations are declining in the eastern US. Despite range overlaps, hybridization has not yet been detected between the native and introduced lineages in the wild, suggesting that phenological or physiological barriers preclude cross-pollination. We demonstrate, for the first time, that native and introduced populations of Phragmites can hybridize. There is substantial overlap in flowering period between native and introduced populations from the same geographic locations. We manually cross-pollinated native individuals with pollen from introduced Phragmites and recovered viable offspring. We then used microsatellite markers to prove that alleles unique to the pollen parent were transferred to progeny. Our results imply a mechanism for the further decline of native Phragmites in North America and a potential for the formation of aggressive hybrid offspring

Hybridization of invasive \u3ci\u3ePhragmites australis\u3c/i\u3e with a native subspecies in North America

Interspecific hybridization can lead to the extinction of native populations and increased aggressiveness in hybrid forms relative to their parental lineages. However, interbreeding among subspecies is less often recognized as a serious threat to native species. Phragmites australis offers an excellent opportunity to investigate intraspecific hybridization since both native and introduced lineages occur in North America. Introduced Phragmites is a highly successful estuarine plant invader throughout North America, but native Phragmites populations are declining in the eastern US. Despite range overlaps, hybridization has not yet been detected between the native and introduced lineages in the wild, suggesting that phenological or physiological barriers preclude cross-pollination. We demonstrate, for the first time, that native and introduced populations of Phragmites can hybridize. There is substantial overlap in flowering period between native and introduced populations from the same geographic locations. We manually cross-pollinated native individuals with pollen from introduced Phragmites and recovered viable offspring. We then used microsatellite markers to prove that alleles unique to the pollen parent were transferred to progeny. Our results imply a mechanism for the further decline of native Phragmites in North America and a potential for the formation of aggressive hybrid offspring

Biogeography of a plant invasion: drivers of latitudinal variation in enemy release

© 2016 John Wiley & Sons Ltd Aim: The relationship between herbivory and latitude may differ between native and invasive plant taxa, which can generate biogeographical heterogeneity in the strength of enemy release. Our aim was to compare latitudinal gradients in herbivory between native and invasive plants and investigate whether gradients are driven by local adaptation or phenotypic plasticity. Location: North America. Methods: Using sympatric native and invasive lineages of the wetland grass Phragmites australis and the specialist gall-fly Lipara rufitarsis, we conducted a field survey to examine whether the relationship between herbivory (the proportion of stems galled) and latitude was parallel between lineages. In a subsequent common garden experiment, we assessed whether latitudinal gradients in herbivory were genetically based or driven by phenotypic plasticity. Results: In the field, L. rufitarsis herbivory on the native P. australis lineage increased from 27% of stems galled in southern populations (36.5°) to 37% in northern populations (43.6°), whereas there was no relationship for the invasive lineage. Similar relationships were evident in the common garden experiment, indicating a genetic basis to latitudinal variation in herbivory. Moreover, the invasive lineage suffered five times less herbivory than the native lineage on average, supporting the enemy release hypothesis. However, a genetic basis to this pattern was absent in the common garden experiment, suggesting that local environmental conditions were responsible for the enemy release observed in nature. Specifically, stem height, diameter and density during the L. rufitarsis oviposition period appeared to be important drivers of herbivory. Main conclusions: Non-parallel gradients in herbivory may help explain the equivocal results of other studies that examine enemy release and biotic resistance at local scales, and can be an important mechanism promoting biogeographical variation in invasion success. We suggest that these latitudinal patterns in herbivory and other species interactions are likely to be a common phenomenon across a range of invaded systems

Allele-Specific Amplification in Cancer Revealed by SNP Array Analysis

Amplification, deletion, and loss of heterozygosity of genomic DNA are hallmarks of cancer. In recent years a variety of studies have emerged measuring total chromosomal copy number at increasingly high resolution. Similarly, loss-of-heterozygosity events have been finely mapped using high-throughput genotyping technologies. We have developed a probe-level allele-specific quantitation procedure that extracts both copy number and allelotype information from single nucleotide polymorphism (SNP) array data to arrive at allele-specific copy number across the genome. Our approach applies an expectation-maximization algorithm to a model derived from a novel classification of SNP array probes. This method is the first to our knowledge that is able to (a) determine the generalized genotype of aberrant samples at each SNP site (e.g., CCCCT at an amplified site), and (b) infer the copy number of each parental chromosome across the genome. With this method, we are able to determine not just where amplifications and deletions occur, but also the haplotype of the region being amplified or deleted. The merit of our model and general approach is demonstrated by very precise genotyping of normal samples, and our allele-specific copy number inferences are validated using PCR experiments. Applying our method to a collection of lung cancer samples, we are able to conclude that amplification is essentially monoallelic, as would be expected under the mechanisms currently believed responsible for gene amplification. This suggests that a specific parental chromosome may be targeted for amplification, whether because of germ line or somatic variation. An R software package containing the methods described in this paper is freely available at http://genome.dfci.harvard.edu/~tlaframb/PLASQ

AXL modulates extracellular matrix protein expression and is essential for invasion and metastasis in endometrial cancer

The receptor tyrosine kinase AXL promotes migration, invasion, and metastasis. Here, we evaluated the role of AXL in endometrial cancer. High immunohistochemical expression of AXL was found in 76% (63/83) of advanced-stage, and 77% (82/107) of high-grade specimens and correlated with worse survival in uterine serous cancer patients. In vitro, genetic silencing of AXL inhibited migration and invasion but had no effect on proliferation of ARK1 endometrial cancer cells. AXL-deficient cells showed significantly decreased expression of phospho-AKT as well as uPA, MMP-1, MMP-2, MMP-3, and MMP-9. In a xenograft model of human uterine serous carcinoma with AXL-deficient ARK1 cells, there was significantly less tumor burden than xenografts with control ARK1 cells. Together, these findings underscore the therapeutic potentials of AXL as a candidate target for treatment of metastatic endometrial cancer

Characterizing genomic alterations in cancer by complementary functional associations.

Systematic efforts to sequence the cancer genome have identified large numbers of mutations and copy number alterations in human cancers. However, elucidating the functional consequences of these variants, and their interactions to drive or maintain oncogenic states, remains a challenge in cancer research. We developed REVEALER, a computational method that identifies combinations of mutually exclusive genomic alterations correlated with functional phenotypes, such as the activation or gene dependency of oncogenic pathways or sensitivity to a drug treatment. We used REVEALER to uncover complementary genomic alterations associated with the transcriptional activation of β-catenin and NRF2, MEK-inhibitor sensitivity, and KRAS dependency. REVEALER successfully identified both known and new associations, demonstrating the power of combining functional profiles with extensive characterization of genomic alterations in cancer genomes

The collapse of intermediate structures?

How can we explain the rise of President Trump and the attraction of his campaign behavior before and since he took office? We argue here that the collapse of ‘intermediate structures’ has been a key factor; that the associations and groups which are building blocks of pluralistic politics have been eroded to such an extent that Trump’s personality politics have been able to take over the political stage