Associations between Psychopathology in Mothers, Fathers and Their Children: A Structural Modeling Approach.

This study investigated associations between parental and child psychopathology with parenting stress as a possible mediator, in order to get more insight in mothers' and fathers' roles in the development of psychopathology in children. Parents of 272 clinically referred (aged 6-20, 66% boys) reported about their own and their child's behavioral problems, and about parenting stress. Data were analyzed using Structural Equation Modeling. Outcomes of path models demonstrated that mothers' higher internalizing and externalizing problems were associated with respectively children's higher internalizing and externalizing problems. Fathers' higher externalizing problems were associated with both children's higher internalizing and externalizing problems, but fathers' internalizing problems were only associated with children's lower externalizing problems. Parenting stress fully mediated the relation between mothers' and children's externalizing problems, and partly mediated the relation between mothers' and children's internalizing problems. For fathers, parenting stress partly mediated the relation between fathers' internalizing problems and children's externalizing problems. Findings indicate that for mothers, the association between parental and child psychopathology is specific, whereas for fathers it is non-specific. Furthermore, results suggest that reducing parenting stress may decrease child problem behavior. Longitudinal studies are needed in order to gain more insight in the direction and underlying mechanisms of the relation between parental and child psychopathology, including parental stress.

AXL and AXR1 have redundant functions in RUB conjugation and growth and development in Arabidopsis.

Cullin-RING ubiquitin-protein ligases such as the Skp1, cullin, F-box protein (SCF) have been implicated in many growth and developmental processes in plants. Normal SCF function requires that the CUL1 subunit be post-translationally modified by related to ubiquitin (RUB), a protein related to ubiquitin. This process is mediated by two enzymes: the RUB-activating and RUB-conjugating enzymes. In Arabidopsis, the RUB-activating enzyme is a heterodimer consisting of AXR1 and ECR1. Mutations in the AXR1 gene result in a pleiotropic phenotype that includes resistance to the plant hormone auxin. Here we report that the AXL (AXR1-like) gene also functions in the RUB conjugation pathway. Overexpression of AXL in the axr1-3 background complements the axr1-3 phenotype. Biochemical analysis indicates that AXL overexpression restores CUL1 modification to the wild-type level, indicating that AXR1 and AXL have the same biochemical activity. Although the axl mutant resembles wild-type plants, the majority of axr1 axl-1 double mutants are embryo or seedling lethal. Furthermore, the axl-1 mutation reveals novel RUB-dependent processes in embryo development. We conclude that AXR1 and AXL function redundantly in the RUB conjugating pathway.

Seed development: Early paternal gene activity in Arabidopsis.

Both parental genomes are expressed during embryogenesis, although the time of activation of the paternally inherited genes varies between organisms. Results reported by Vielle-Calzada et al. have suggested that delayed activation of the paternal genome seems to be the rule in plant development. We find, however, that during early embryogenesis in Arabidopsis, paternal genes are expressed and are sufficient for normal development. Our findings indicate that there is no overall maternal control of early embryogenesis, and that the contribution of the parental alleles needs to be assessed for each gene individually.

An Arabidopsis Minute-like phenotype caused by a semi-dominant mutation in a RIBOSOMAL PROTEIN S5 gene.

Mutations in ribosomal protein (RP) genes in Drosophila lead to strong developmental phenotypes, expressed in the semi-dominant Minute syndrome. In plants, however, mutations in RP genes have so far only been reported to result in recessive developmental phenotypes. We present the analysis of an Arabidopsis promoter-trap line, in which a T-DNA insertion in an RPS5 gene (AtRPS5A) causes semi-dominant developmental phenotypes. Most cell-division processes are delayed or disturbed in the heterozygous mutant, and development is completely arrested at an early embryonic stage in the homozygous mutant. By analogy with Drosophila rp mutants, we have named this mutant Arabidopsis Minute-like 1 (aml1). As with other Arabidopsis RPs, RPS5 is represented by a small gene family, but in contrast to other described plant RPs, this family comprises only two members. The AtRPS5A gene (mutated in aml1) is strongly expressed in dividing cells, whereas expression of the second RPS5 gene, AtRPS5B, is lower than that of AtRPS5A, and is correlated with cell differentiation rather than cell division. From expression analyses we conclude that AtRPS5A is the most abundantly expressed RPS5 gene in Arabidopsis. The Minute-like defects in the aml1 mutant provide the first evidence that ribosome insufficiency leads to similar consequences in both plants and insects, and emphasize the general importance of efficient protein translation for cell proliferation in higher eukaryotes.

The PINOID protein kinase regulates organ development in Arabidopsis by enhancing polar auxin transport.

Arabidopsis pinoid mutants show a strong phenotypic resemblance to the pin-formed mutant that is disrupted in polar auxin transport. The PINOID gene was recently cloned and found to encode a protein-serine/threonine kinase. Here we show that the PINOID gene is inducible by auxin and that the protein kinase is present in the primordia of cotyledons, leaves and floral organs and in vascular tissue in developing organs or proximal to meristems. Overexpression of PINOID under the control of the constitutive CaMV 35S promoter (35S::PID) resulted in phenotypes also observed in mutants with altered sensitivity to or transport of auxin. A remarkable characteristic of high expressing 35S::PID seedlings was a frequent collapse of the primary root meristem. This event triggered lateral root formation, a process that was initially inhibited in these seedlings. Both meristem organisation and growth of the primary root were rescued when seedlings were grown in the presence of polar auxin transport inhibitors, such as naphthylphtalamic acid (NPA). Moreover, ectopic expression of PINOID cDNA under control of the epidermis-specific LTP1 promoter provided further evidence for the NPA-sensitive action of PINOID. The results presented here indicate that PINOID functions as a positive regulator of polar auxin transport. We propose that PINOID is involved in the fine-tuning of polar auxin transport during organ formation in response to local auxin concentrations.