Pruning reduces blister rust in sugar pine with minimal effects on tree growth

Sugar pine trees from nine stands in two California study areas were assessed to determine the effects of pruning on the incidence and growth of white pine blister rust. Lower limbs up to 8 feet high were removed on alternate trees. Six years following treatment, the number of infections in pruned trees was reduced compared to unpruned trees at one study area, but no blister rust was found at the other area. The results suggest that artificial pruning of sugar pine may be part of an effective, integrated strategy to maintain this species in mixed-conifer California forests

Identification of habitat controls on northern red-legged frog populations: implications for habitat conservation on an urbanizing landscape in the Pacific Northwest

Abstract Introduction In the Pacific Northwest of North America, research addressing lentic-breeding amphibian population vulnerability has emphasized aquatic habitats, frequently neglecting terrestrial habitats. Consequently, wetland protection and restoration often fails to preserve or restore adjacent uplands required by lentic-breeding amphibians. Inattention to the juxtaposition and connectivity of uplands to wetlands could locally extirpate lentic-breeding amphibians. The objective of this research is to identify the relative importance of juxtaposed terrestrial and aquatic habitats in a lentic-breeding amphibian, the northern red-legged frog (Rana aurora), by evaluating the relationship between its occurrence and abundance with its aquatic and terrestrial habitats. To accomplish this, egg mass counts were used to quantify R. aurora populations in 30 stillwater habitats across an urbanization gradient. Using a Geographic Information System, seven descriptors of aquatic and surrounding terrestrial habitats were measured to evaluate their relationships to R. aurora occurrence and abundance. Results Rana aurora occurrence and breeding abundance both reflect the forested area around wetland breeding sites and forest connectivity to those sites. Rana aurora breeding abundance also strongly reflects the percent of forested perimeter around wetland breeding sites. The forest habitat most important for R. aurora breeding abundance seems to be > 200 m from the breeding wetlands. The American bullfrog presence and the two aquatic parameters measured, wetland area and vegetated area, were unrelated to R. aurora occurrence and breeding abundance. Conclusions Area and connectivity of juxtaposed forested terrestrial habitat may represent a basic control on R. aurora presence and population size. Urban development policies should consider preservation and restoration of upland forest habitats beyond current fixed-width buffers and wetland habitat area at landscape scales

FOXC2 promotes vasculogenic mimicry and resistance to anti-angiogenic therapy.

Vasculogenic mimicry (VM) describes the formation of pseudo blood vessels constructed of tumor cells that have acquired endothelial-like properties. VM channels endow the tumor with a tumor-derived vascular system that directly connects to host blood vessels, and their presence is generally associated with poor patient prognosis. Here we show that the transcription factor, Foxc2, promotes VM in diverse solid tumor types by driving ectopic expression of endothelial genes in tumor cells, a process that is stimulated by hypoxia. VM-proficient tumors are resistant to anti-angiogenic therapy, and suppression of Foxc2 augments response. This work establishes co-option of an embryonic endothelial transcription factor by tumor cells as a key mechanism driving VM proclivity and motivates the search for VM-inhibitory agents that could form the basis of combination therapies with anti-angiogenics

SPEN haploinsufficiency causes a neurodevelopmental disorder overlapping proximal 1p36 deletion syndrome with an episignature of X chromosomes in females

Deletion 1p36 (del1p36) syndrome is the most common human disorder resulting from a terminal autosomal deletion. This condition is molecularly and clinically heterogeneous. Deletions involving two non-overlapping regions, known as the distal (telomeric) and proximal (centromeric) critical regions, are sufficient to cause the majority of the recurrent clinical features, although with different facial features and dysmorphisms. SPEN encodes a transcriptional repressor commonly deleted in proximal del1p36 syndrome and is located centromeric to the proximal 1p36 critical region. Here, we used clinical data from 34 individuals with truncating variants in SPEN to define a neurodevelopmental disorder presenting with features that overlap considerably with those of proximal del1p36 syndrome. The clinical profile of this disease includes developmental delay/intellectual disability, autism spectrum disorder, anxiety, aggressive behavior, attention deficit disorder, hypotonia, brain and spine anomalies, congenital heart defects, high/narrow palate, facial dysmorphisms, and obesity/increased BMI, especially in females. SPEN also emerges as a relevant gene for del1p36 syndrome by co-expression analyses. Finally, we show that haploinsufficiency of SPEN is associated with a distinctive DNA methylation episignature of the X chromosome in affected females, providing further evidence of a specific contribution of the protein to the epigenetic control of this chromosome, and a paradigm of an X chromosome-specific episignature that classifies syndromic traits. We conclude that SPEN is required for multiple developmental processes and SPEN haploinsufficiency is a major contributor to a disorder associated with deletions centromeric to the previously established 1p36 critical regions.The article is available via Open Access. Click on the 'Additional link' above to access the full-text.Published version, accepted version (6 month embargo), submitted versio

SPEN haploinsufficiency causes a neurodevelopmental disorder overlapping proximal 1p36 deletion syndrome with an episignature of X chromosomes in females

Deletion 1p36 (del1p36) syndrome is the most common human disorder resulting from a terminal autosomal deletion. This condition is molecularly and clinically heterogeneous. Deletions involving two non-overlapping regions, known as the distal (telomeric) and proximal (centromeric) critical regions, are sufficient to cause the majority of the recurrent clinical features, although with different facial features and dysmorphisms. SPEN encodes a transcriptional repressor commonly deleted in proximal del1p36 syndrome and is located centromeric to the proximal 1p36 critical region. Here, we used clinical data from 34 individuals with truncating variants in SPEN to define a neurodevelopmental disorder presenting with features that overlap considerably with those of proximal del1p36 syndrome. The clinical profile of this disease includes developmental delay/intellectual disability, autism spectrum disorder, anxiety, aggressive behavior, attention deficit disorder, hypotonia, brain and spine anomalies, congenital heart defects, high/narrow palate, facial dysmorphisms, and obesity/increased BMI, especially in females. SPEN also emerges as a relevant gene for del1p36 syndrome by co-expression analyses. Finally, we show that haploinsufficiency of SPEN is associated with a distinctive DNA methylation episignature of the X chromosome in affected females, providing further evidence of a specific contribution of the protein to the epigenetic control of this chromosome, and a paradigm of an X chromosome-specific episignature that classifies syndromic traits. We conclude that SPEN is required for multiple developmental processes and SPEN haploinsufficiency is a major contributor to a disorder associated with deletions centromeric to the previously established 1p36 critical regions