Resistance against herbicide isoxaben and cellulose deficiency caused by distinct mutations in same cellulose synthase isoform CESA6

Isoxaben is a pre-emergence herbicide that inhibits cellulose biosynthesis in higher plants. Two loci identified by isoxaben-resistant mutants (ixr1-1, ixr1-2, and ixr2-1) in Arabidopsis have been reported previously. IXR1 was recently shown to encode the cellulose synthase catalytic subunit CESA3 (W.-R. Scheible, R. Eshed, T. Richmond, D. Delmer, and C. Somerville [2001] Proc Natl Acad Sci USA 98: 10079-10084). Here, we report on the cloning of IXR2, and show that it encodes another cellulose synthase isoform, CESA6. ixr2-1 carries a mutation substituting an amino acid close to the C terminus of CESA6 that is highly conserved among CESA family members. Transformation of wild-type plants with the mutated gene and not with the wild-type gene conferred increased resistance against the herbicide. The simplest interpretation for the existence of these two isoxaben-resistant loci is that CESA3 and CESA6 have redundant functions. However, loss of function procuste1 alleles of CESA6 were previously shown to have a strong growth defect and reduced cellulose content in roots and dark-grown hypocotyls. This indicates that in these mutants, the presence of CESA3 does not compensate for the absence of CESA6 in roots and dark-grown hypocotyls, which argues against redundant functions for CESA3 and CESA6. Together, these observations are compatible with a model in which CESA6 and CESA3 are active as a protein complex.     

Regulation of clusterin expression in mammary epithelial cells

Mammary epithelial cells undergo changes in growth, invasion, differentiation, and dedifferentiation throughout much of adult hood, and most strikingly during pregnancy, lactation, and involution. Clusterin is a multifunctional glycoprotein that is involved in the differentiation and morphogenesis of epithelia, and that is important in the regulation of postnatal mammary gland development. However, the mechanisms that regulate clusterin expression are still poorly understood. Here, we show that clusterin is up-regulated twice during mouse mammary gland development, a first time at the end of pregnancy and a second time at the beginning of the involution. These points of clusterin up-regulation coincide with the dramatic phenotypic and functional changes occurring in the mammary gland. Using cell culture conditions that resemble the regulatory microenvironment in vivo, we determined that the factors responsible for the first up-regulation of clusterin levels can include the extracellular matrix component, laminin, and the lactogenic hormones, prolactin and hydrocortisone. On the other hand, the second and most dramatic up-regulation of clusterin can be due to the potent induction by TGF-beta1, and this up-regulation by TGF-beta1 is dependent on beta1 integrin ligand-binding activity. Moreover, the level of expression of beta-casein, a marker of mammary epithelial cell differentiation, was decreased upon treatment of cells with clusterin siRNA. Overall, these findings reveal several novel pathways for the regulation of clusterin expression during mammary gland development, and suggest that clusterin is a morphogenic factor that plays a key role during differentiation.     

Receptor Kinase THESEUS1 Is a Rapid Alkalinization Factor 34 Receptor in Arabidopsis

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Fluctuations naturelles et évolution artificielle des biocénoses macrozoobenthiques intertidales de trois estuaires des côtes françaises de la Manche

The study of the intertidal benthic population dynamics in three estuaries of the English Channel (Baie des Veys, Seine estuary, Baie de Somme:France) brings to light two types of species:

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key-species which directly respond to the local disturbance of the environmental conditions in their densities (Spionidae, Capitellidae) and in their growth rates (Cerastoderma edule);

target-species such as Macoma balthica which can endure brief changes in the environmental factors and shows no sign of long-lasting consequences on its population dynamics; yet, it fully integrates long-term changes through its numbers and productivity.

The parallel between such a regular study of the seasonal variations on selected sites and various base line surveys allows the authors to discuss the COST 647 sampling programm in order to selectrms, range of temperature) from human disturbances (embankments, chemical pollution, eutrophication). Diverse hypothesis are suggested which bring about several research topics to be developed within a european cooperation.     

Age-specific cost of first reproduction in female southern elephant seals

When to commence breeding is a crucial life-history decision that may be the most important determinant of an individual''s lifetime reproductive output and can have major consequences on population dynamics. The age at which individuals first reproduce is an important factor influencing the intensity of potential costs (e.g. reduced survival) involved in the first breeding event. However, quantifying age-related variation in the cost of first reproduction in wild animals remains challenging because of the difficulty in reliably recording the first breeding event. Here, using a multi-event capture–recapture model that accounts for both imperfect detection and uncertainty in the breeding status on an 18-year dataset involving 6637 individuals, we estimated age and state-specific survival of female elephant seals (Mirounga leonina) in the declining Macquarie Island population. We detected a clear cost of first reproduction on survival. This cost was higher for both younger first-time breeders and older first-time breeders compared with females recruiting at age four, the overall mean age at first reproduction. Neither earlier primiparity nor delaying primiparity appear to confer any evolutionary advantage, rather the optimal strategy seems to be to start breeding at a single age, 4 years.     

Drought effects on damage by forest insects and pathogens: a meta‐analysis

In the context of climate change, the effects of prolonged or more severe droughts on pest and pathogen damage are a major concern for forest ecosystems. To date, there is great uncertainty about the direction, magnitude and sources of variation in responses to drought by insects and fungi. We report the outcomes of a meta‐analysis of 100 pairwise comparisons of insect pest or pathogen damage to water‐stressed and control trees from 40 publications. The type of feeding substrate for insects and fungi and the water stress severity emerged as the main factors influencing the level of damage in water‐stressed trees. Overall, primary damaging agents living in wood caused significantly lower damage to the water‐stressed trees compared with the control, whereas primary pests and pathogens living on foliage caused more damage to water‐stressed trees, in all cases irrespective of stress severity. In contrast, damage by secondary agents increased with stress severity, which was best estimated by the ratio between the predawn leaf water potential in stressed trees and the xylem pressure inducing 50% loss in hydraulic conductance due to cavitation, a species‐specific index of drought tolerance. Insect and fungus feeding behaviour, affected tree part, and water stress severity are therefore proposed as three important predictors of forest damage in drought conditions.     

A role for p53 in maintaining and establishing the quiescence growth arrest in human cells

The p53 tumor suppressor protein induces transient growth arrest or apoptosis in response to genotoxic stress and mediates the irreversible growth arrest of cellular senescence. We present evidence here that p53 also contributes to the reversible, growth factor-dependent arrest of quiescence (G(0)). Microinjection of expression vectors encoding either MDM2 or a pRb-binding mutant of SV40 T antigen, both of which abrogate p53 function, stimulated quiescent normal human fibroblasts to initiate DNA synthesis and were 40-70% as effective as wild-type T antigen. Electrophoretic mobility shift and p53 transactivation assays showed that p53 activity was higher in quiescent and senescent cells compared with proliferating cells. As proliferating cells entered G(0) after growth factor withdrawal, the p53 mRNA level increased, followed by transient accumulation of the protein. Shortly thereafter, the expression (mRNA and protein) of p21, a p53 target gene and effector of cell cycle arrest, increased. Finally, stable expression of the HPV16 E6 oncogene or dominant negative p53 peptide, GSE-22, both of which inhibit p53 function, delayed entry into quiescence following growth factor withdrawal. Our data indicate that p53 is activated during both quiescence and senescence. They further suggest that p53 activity contributes, albeit not exclusively, to the quiescent growth arrest.