Climate lags and genetics determine phenology in quaking aspen (Populus tremuloides).

Spatiotemporal patterns of phenology may be affected by mosaics of environmental and genetic variation. Environmental drivers may have temporally lagged impacts, but patterns and mechanisms remain poorly known. We combine multiple genomic, remotely sensed, and physically modeled datasets to determine the spatiotemporal patterns and drivers of canopy phenology in quaking aspen, a widespread clonal dioecious tree species with diploid and triploid cytotypes. We show that over 391 km2 of southwestern Colorado: greenup date, greendown date, and growing season length vary by weeks and differ across sexes, cytotypes, and genotypes; phenology has high phenotypic plasticity and heritabilities of 31-61% (interquartile range); and snowmelt date, soil moisture, and air temperature predict phenology, at temporal lags of up to 3 yr. Our study shows that lagged environmental effects are needed to explain phenological variation and that the effect of cytotype on phenology is obscured by its correlation with topography. Phenological patterns are consistent with responses to multiyear accumulation of carbon deficit or hydraulic damage.

Remote sensing of cytotype and its consequences for canopy damage in quaking aspen.

Mapping geographic mosaics of genetic variation and their consequences via genotype x environment interactions at large extents and high resolution has been limited by the scalability of DNA sequencing. Here, we address this challenge for cytotype (chromosome copy number) variation in quaking aspen, a drought-impacted foundation tree species. We integrate airborne imaging spectroscopy data with ground-based DNA sequencing data and canopy damage data in 391 km2 of southwestern Colorado. We show that (1) aspen cover and cytotype can be remotely sensed at 1 m spatial resolution, (2) the geographic mosaic of cytotypes is heterogeneous and interdigitated, (3) triploids have higher leaf nitrogen, canopy water content, and carbon isotope shifts (δ13 C) than diploids, and (4) canopy damage varies among cytotypes and depends on interactions with topography, canopy height, and trait variables. Triploids are at higher risk in hotter and drier conditions.

Cytotype and genotype predict mortality and recruitment in Colorado quaking aspen (Populus tremuloides).

Species responses to climate change depend on environment, genetics, and interactions among these factors. Intraspecific cytotype (ploidy level) variation is a common type of genetic variation in many species. However, the importance of intraspecific cytotype variation in determining demography across environments is poorly known. We studied quaking aspen (Populus tremuloides), which occurs in diploid and triploid cytotypes. This widespread tree species is experiencing contractions in its western range, which could potentially be linked to cytotype-dependent drought tolerance. We found that interactions between cytotype and environment drive mortality and recruitment across 503 plots in Colorado. Triploids were more vulnerable to mortality relative to diploids and had reduced recruitment on more drought-prone and disturbed plots relative to diploids. Furthermore, there was substantial genotype-dependent variation in demography. Thus, cytotype and genotype variation are associated with decline in this foundation species. Future assessment of demographic responses to climate change will benefit from knowledge of how genetic and environmental mosaics interact to determine species' ecophysiology and demography.

Patients with B cell chronic lymphocytic leukaemia have an expanded population of CD4 perforin expressing T cells enriched for human cytomegalovirus specificity and an effector-memory phenotype.

We have previously shown an expansion of cytotoxic antigen-experienced CD4(+)T cells (CTLs) that express perforin (PF) in the peripheral blood of patients with B cell chronic lymphocytic leukaemia (B-CLL). Increased frequencies of CD4(+)CTLs have since been attributed to chronic viral infections, particularly, human cytomegalovirus (HCMV). The present study examined the involvement of CD4(+)CTLs in responses to HCMV in B-CLL, and characterized their differentiation. We studied 36 HCMV seropositive (SP) and seronegative B-CLL patients and 20 healthy age-matched individuals. The HCMV reactivity of CD4(+)PF(+) and CD4(+)PF(-) cells was determined by interferon-gamma expression, and expression of CD45RA and CCR7 was assessed by flow cytometry. Fluorescence in-situ hybridization was used to measure relative telomere lengths. CD4(+)PF(+)T cell expansion in B-CLL patients and controls was strongly associated with HCMV seropositivity. CD4(+)PF(+) compared to CD4(+)PF(-) cells from SP B-CLL patients elicited major histocompatibility complex (MHC) class II-restricted responses to HCMV. CD4(+)PF(+)T cells from patients and controls were enriched with highly differentiated T-effector/memory (CCR7(-)) and revertant (CCR7(-)CD45RA(+)) phenotype. CD4(+)PF(+)T cells from B-CLL patients had shorter telomeres than CD4(+)PF(-)T cells, indicating an extensive replicative history. We conclude that persistent exposure to HCMV antigens in SP B-CLL patients leads to an expansion of the circulating MHC class II-restricted CD4(+)PF(+)T cell population with effector/memory phenotype.