Physiological and molecular adaptation mechanisms enable plants to improve their survival under harsh conditions, including low oxygen levels caused by flooding. When Arabidopsis was exposed to hypoxia, we observed hyponastic response, shoot elongation, leaf chlorosis, and inhibited growth. To understand this response, we used a specialized complementary DNA microarray from our laboratory to examine the time-dependent profiles of gene expression in Arabidopsis roots and shoots. From this, we identified 282 hypoxia-responsive genes. These included novel genes for a zinc finger protein, WRKY family transcription factor, and glycosyl hydrolase as well as those previously identified as hypoxia-related genes including alcohol dehydrogenase (ADH), pyruvate decarboxylase (PDC), and phosphofructokinase. Cluster analysis of these profiles suggested that the hypoxia response occurs in two distinctive phases: early and late. The early response to imposed stress (hours 1, 3, and 8) includes increased expression of fermentation-related genes and transcription factors, such as by members of the C 2 H 2 zinc finger family and WRKY family. The late response (hours 24 and 72) involves the down-regulation of genes that function in secondary metabolic pathways and up-regulation of transcription factors that are mostly related to the ethylene-responsive element binding protein family. Mutants of Arabidopsis defective in sucrose synthase1 (SUS1), the At1g05060 gene (with unknown function), ADH, and the WRKY33 were more sensitive to hypoxic stress, evidence of the importance of these genes in that response. The genes presented here allow us to deepen our understanding of the mechanism for this stress response and, eventually, will aid in the development of more flood-tolerant crops.
Chromosomal abnormalities are implicated in a substantial number of human developmental syndromes, but for many such disorders little is known about the causative genes. The recently described 1q41q42 microdeletion syndrome is characterized by characteristic dysmorphic features, intellectual disability and brain morphological abnormalities, but the precise genetic basis for these abnormalities remains unknown. Here, our detailed analysis of the genetic abnormalities of 1q41q42 microdeletion cases identified TP53BP2, which encodes apoptosis-stimulating protein of p53 2 (ASPP2), as a candidate gene for brain abnormalities. Consistent with this, Trp53bp2-deficient mice show dilation of lateral ventricles resembling the phenotype of 1q41q42 microdeletion patients. Trp53bp2 deficiency causes 100% neonatal lethality in the C57BL/6 background associated with a high incidence of neural tube defects and a range of developmental abnormalities such as congenital heart defects, coloboma, microphthalmia, urogenital and craniofacial abnormalities. Interestingly, abnormalities show a high degree of overlap with 1q41q42 microdeletion-associated abnormalities. These findings identify TP53BP2 as a strong candidate causative gene for central nervous system (CNS) defects in 1q41q42 microdeletion syndrome, and open new avenues for investigation of the mechanisms underlying CNS abnormalities.
Cold acclimation enables plants to withstand low but non-freezing temperatures. Biochemical and physiological changes include a reduction in tissue water content and altered composition of membrane lipids. These responses are correlated with fluctuations in the expression of coldinduced genes such as LTI (low-temperature-induced), KIN (cold-inducible), RD (responsive to desiccation), and ERD (early dehydration-inducible). We performed time-course experiments with specialized cDNA microarrays comprising 712 cDNAs selected by SAGE and SSH methods. Expression dynamics were monitored in the leaves of Arabidopsis. Profiles of nine samples from plants chilled for various time periods revealed 264 cold-inducible genes and 33 repressed genes, for which expression was altered (up or down) by at least twofold. These included not only several previously reported cold-regulated genes, e.g., rd, lea, and CBF3, but also candidate genes such as those for alcohol dehydrogenase and transport inhibitor response 1. All genes were grouped according to their expression patterns; most tended to shift their expression at 3∼8 h after cold treatment. Two cold-associated transcriptional activators, CBF2 and CBF3, did not have parallel patterns of expression, although both were induced within 15 min. Our results suggest different roles for CBF2 and CBF3 in the signaltransduction pathway for cold acclimation. We believe that, compared with standard differential screening, our microarray analysis is a more useful technique for the selection of new candidate genes responsible for cold acclimation.
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