We studied the hydraulic architecture and water relations of nine co-occurring woody species in a Spanish evergreen oak forest over the course of a dry season. Our main objectives were to: (1) test the existence of a trade-off between hydraulic conductivity and security in the xylem, and (2) establish the safety margins at which the species operated in relation to hydraulic failure, and compare these safety margins between species and tissues (roots vs. stems). Our results showed that the relationship between specific hydraulic conductivity (K s) and resistance to cavitation followed a power function with exponent ≈-2, consistent with the existence of a trade-off between conductivity and security in the xylem, and also consistent with a linear relationship between vessel diameter and the size of inter-vessel pores. The diameter of xylem conduits, K s and vulnerability to xylem embolism were always higher in roots than in stems of the same species. Safety margins from hydraulic failure were narrower in roots than in stems. Among species, the water potential (Ψ) at which 50% of conductivity was lost due to embolism ranged between -0.9 and <-8 MPa for roots and between -2.0 and <-8 MPa for stems. Vulnerability to xylem embolism followed a pattern of: Quercus ilex=Acer monspessulanum=Arbutus unedo=Sorbus torminalis=Cistus laurifolius>Cistus albidus=Ilex aquifolium>Phillyrea latifolia>Juniperus oxycedrus. Gas exchange and seasonal Ψ minima were in general correlated with resistance to xylem embolism. Hydraulic safety margins differed markedly among species, with some of them (J. oxycedrus, I. aquifolium, P. latifolia) showing a xylem overly resistant to cavitation. We hypothesize that this overly resistant xylem may be related to the shape of the relationship between K s and security we have found.

Genomic copy number changes are frequently found in cancers and they have been demonstrated to contribute to carcinogenesis; and it is widely accepted that tumors with microsatellite instability (MSI) are genetically stable and mostly diploid. In the present study we compared the copy number alterations and the gene-expression profiles of microsatellite stable (MSS) and MSI colorectal tumors. A total number of 31 fresh-frozen primary tumors (16 MSS and 15 MSI) were used. Twenty-eight samples (15 MSS and 13 MSI) were analyzed with metaphase comparative genomic hybridization (CGH), nine of which plus one additional sample (4 MSS and 6 MSI) were further analyzed by cDNA-based array-CGH. Gene expression analysis was performed with six samples [3 MSS and 3 MSI, four of these used in metaphase CGH (mCGH) analysis] to identify differentially expressed genes possibly located in the lost or amplified regions found by CGH, stressing the biological significance of copy number changes. Metaphase and array-CGH analysis of two colon cancer cell lines (HTC116 and SW480, reported as MSI and MSS archetypes) gave comparable results. Alterations found by mCGH in MSS tumors were +20, +8q, -8p and -18q. Interestingly, 1p22, 4q26 and 15q21 were found deleted preferentially in MSS tumors, while 22q13 was found gained in MSI tumors. The regions of alterations identified by array-CGH were gains at 8q24, 16q24.3 and 20q13, and the loss of 5q21, appearing in the both types of tumors. Gene expression analysis revealed genes with specific associations with the copy number changes of the corresponding genomic regions. As a conclusion, colorectal cancer is a heterogeneous disease, demonstrated by the genomic profiles of individual samples. However, our data shows that copy number changes do not occur exclusively in the MSS phenotypes.

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