A longer wood growing season does not lead to higher carbon sequestration.

A reliable assessment of forest carbon sequestration depends on our understanding of wood ecophysiology. Within a forest, trees exhibit different timings and rates of growth during wood formation. However, their relationships with wood anatomical traits remain partially unresolved. This study evaluated the intra-annual individual variability in growth traits in balsam fir [Abies balsamea (L.) Mill.]. We collected wood microcores weekly from April to October 2018 from 27 individuals in Quebec (Canada) and prepared anatomical sections to assess wood formation dynamics and their relationships with the anatomical traits of the wood cells. Xylem developed in a time window ranging from 44 to 118 days, producing between 8 and 79 cells. Trees with larger cell production experienced a longer growing season, with an earlier onset and later ending of wood formation. On average, each additional xylem cell lengthened the growing season by 1 day. Earlywood production explained 95% of the variability in xylem production. More productive individuals generated a higher proportion of earlywood and cells with larger sizes. Trees with a longer growing season produced more cells but not more biomass in the wood. Lengthening the growing season driven by climate change may not lead to enhanced carbon sequestration from wood production.

Upscaling xylem phenology: sample size matters.

BACKGROUND AND AIMS: Upscaling carbon allocation requires knowledge of the variability at the scales at which data are collected and applied. Trees exhibit different growth rates and timings of wood formation. However, the factors explaining these differences remain undetermined, making samplings and estimations of the growth dynamics a complicated task, habitually based on technical rather than statistical reasons. This study explored the variability in xylem phenology among 159 balsam firs [Abies balsamea (L.) Mill.]. METHODS: Wood microcores were collected weekly from April to October 2018 in a natural stand in Quebec, Canada, to detect cambial activity and wood formation timings. We tested spatial autocorrelation, tree size and cell production rates as explanatory variables of xylem phenology. We assessed sample size and margin of error for wood phenology assessment at different confidence levels. KEY RESULTS: Xylem formation lasted between 40 and 110 d, producing between 12 and 93 cells. No effect of spatial proximity or size of individuals was detected on the timings of xylem phenology. Trees with larger cell production rates showed a longer growing season, starting xylem differentiation earlier and ending later. A sample size of 23 trees produced estimates of xylem phenology at a confidence level of 95 % with a margin of error of 1 week. CONCLUSIONS: This study highlighted the high variability in the timings of wood formation among trees within an area of 1 km2. The correlation between the number of new xylem cells and the growing season length suggests a close connection between the processes of wood formation and carbon sequestration. However, the causes of the observed differences in xylem phenology remain partially unresolved. We point out the need to carefully consider sample size when assessing xylem phenology to explore the reasons underlying this variability and to allow reliable upscaling of carbon allocation in forests.

A pituitary-specific enhancer of the POMC gene with preferential activity in corticotrope cells.

Cell-specific expression of the pituitary proopiomelanocortin (POMC) gene depends on the combination of tissue- and cell-restricted transcription factors such as Pitx1 and Tpit. These factors act on the proximal POMC promoter together with transcription factors that integrate inputs from signaling pathways. We now report the identification of an upstream enhancer in the POMC locus that is targeted by the same subset of transcription factors, except Pitx1. This enhancer located at -7 kb in the mouse POMC gene is highly dependent on Tpit for activity. Whereas Tpit requires Pitx1 for action on the promoter, it acts on the -7-kb enhancer as homodimers binding to a palindromic Tpit response element (TpitRE). Both half-sites of the TpitRE palindrome and Tpit homodimerization are required for activity. In vivo, the enhancer exhibits preferential activity in corticotrope cells of the anterior lobe whereas the promoter exhibits preference for intermediate lobe melanotropes. The enhancer is conserved among different species with the TpitRE palindrome localized at the center of conserved sequences. However, the mouse and human -7-kb enhancers do not exhibit conservation of hormone responsiveness and may differ in their relative importance for POMC expression. In summary, pituitary expression of the POMC gene relies on an upstream enhancer that complements the activity of the proximal promoter with Tpit as the major regulator of both regulatory regions.

Transcriptional control of the ERBB2 amplicon by ERRalpha and PGC-1beta promotes mammary gland tumorigenesis.

Overexpression of ERBB2 and its neighboring genes on chromosome 17 occurs in approximately 25% of breast tumors and is associated with poor prognosis. While amplification of the 17q12-21 chromosomal region often correlates with an increase in the transcriptional rates of the locus, the molecular mechanisms and the factors involved in the coordinated expression of genes residing within the ERBB2 amplicon remain largely unknown. Here we demonstrate that estrogen-related receptor α (ERRα, NR3B1) and its coregulator PGC-1ß are key effectors in this process. Using a mouse model of ERBB2-initiated mammary tumorigenesis, we first show that ablation of ERRα significantly delays ERBB2-induced tumor development and lowers the levels of amplicon transcripts. Chromosome 17q-wide binding site location analyses in human breast cancer cells show preferential recruitment of ERRα to DNA segments associated with the ERBB2 amplicon. Furthermore, ERRα directs the co-recruitment of the coactivator PGC-1ß to segments in the 17q12 region and the recruitment of RNA polymerase II to the promoters of the ERBB2 and coamplified genes. ERRα and PGC-1ß also participate in the de-repression of ERBB2 expression through competitive genomic cross-talk with estrogen receptor α (ERα) and, as a consequence, influence tamoxifen sensitivity in breast cancer cells. Taken together, our results suggest that ERRα and PGC-1ß are key players in the etiology of malignant breast cancer by coordinating the transcriptional regulation of genes located in the 17q12 region, a process that also involves interference with the repressive function of ERα on ERBB2 expression.

An acetylation switch modulates the transcriptional activity of estrogen-related receptor alpha.

Posttranslational modifications are instrumental to achieve gene- and tissue-specific regulatory outcomes by transcription factors. Nuclear receptors are dynamically modulated by several types of posttranslational modifications including phosphorylation, methylation, acetylation, ubiquitination, and sumoylation. The estrogen-related receptor alpha (ERRalpha, NR3B1) is phosphorylated on multiple sites, and sumoylated in the amino-terminal region in a phosphorylation-dependent manner. Here we demonstrate that ERRalpha interacts with and is acetylated by p300 coactivator associated factor (PCAF) in vitro and in mouse liver. Purified PCAF acetylated the DNA-binding domain of ERRalpha on four highly-conserved lysines. In addition, coexpression of PCAF reduced the transcriptional activity of ERRalpha and, reciprocally, a deacetylase screen identified histone deacetylase 8 (HDAC8) and sirtuin 1 homolog (Sirt1) as independent enhancers of ERRalpha transcriptional function. HDAC8 and Sirt1 were also demonstrated to interact directly with ERRalpha in vivo and to deacetylate and increase the DNA binding affinity of ERRalpha in vitro. The removal of PCAF increases the DNA binding of ERRalpha in vivo, whereas the removal of Sirt1 and HDAC8 decreases it as assessed by chromatin immunoprecipitation assay. Altogether, our results show that ERRalpha is an acetylated protein and imply the existence of a dynamic acetylation/deacetylation switch involved in the control of ERRalpha transcriptional activity.