There might be unidentified tumor suppressor genes on chromosome 10q22-10q23 and 22q11.2-22q12.1 that contribute to the pathogenesis and development of HCC.

All over the world, a common problem in the soil is the low content of available zinc (Zn), which is unevenly distributed and difficult to move. However, information on the foraging strategies of roots in response to heterogeneous Zn supply is still very limited. Few studies have analyzed the adaptability of maize inbred lines with different Zn efficiencies to different low Zn stress time lengths in maize. This study analyzed the effects of different time lengths of low Zn stress on various related traits in different inbred lines. In addition, morphological plasticity of roots and the response of Zn-related important gene iron-regulated transporter-like proteins (ZIPs) were studied via simulating the heterogeneity of Zn nutrition in the soil. In this report, when Zn deficiency stress duration was extended (from 14 to 21 days), under Zn-deficient supply (0.5 μM), Zn efficiency (ZE) based on shoot dry weight of Wu312 displayed no significant difference, and ZE for Ye478 was increased by 92.9%. Under longer-term Zn deficiency, shoot, and root dry weights of Ye478 were 6.5 and 2.1-fold higher than those of Wu312, respectively. Uneven Zn supply strongly inhibited the development of some root traits in the -Zn region. Difference in shoot dry weights between Wu312 and Ye478 was larger in T1 (1.97 times) than in T2 (1.53 times). Under heterogeneous condition of Zn supply, both the –Zn region and the +Zn region upregulated the expressions of ZmZIP3, ZmZIP4, ZmZIP5, ZmZIP7, and ZmZIP8 in the roots of two inbred lines. These results indicate that extended time length of low-Zn stress will enlarge the difference of multiple physiological traits, especially biomass, between Zn-sensitive and Zn-tolerant inbred lines. There were significant genotypic differences of root morphology in response to heterogeneous Zn supply. Compared with split-supply with +Zn/+Zn, the difference of above-ground biomass between Zn-sensitive and Zn-tolerant inbred lines under split-supply with –Zn/+Zn was higher. Under the condition of heterogeneous Zn supply, several ZmZIP genes may play important roles in tolerance to low Zn stress, which can provide a basis for further functional characterization.

Zinc (Zn) deficiency, a globally predominant micronutrient disorder in crops and humans, reduces crop yields and adversely impacts human health. Despite numerous studies on the physiological mechanisms underlying Zn deficiency tolerance, its genetic basis of molecular mechanism is still poorly understood. Thus, the Zn efficiency of 20 maize inbred lines was evaluated, and a quantitative trait locus (QTL) analysis was performed in the recombination inbred line population derived from the most Zn-efficient (Ye478) and Zn-inefficient inbred line (Wu312) to identify the candidate genes associated with Zn deficiency tolerance. On this basis, we analyzed the expression of ZmZIP1-ZmZIP8. Thirteen QTLs for the traits associated with Zn deficiency tolerance were detected, explaining 7.6–63.5% of the phenotypic variation. The genes responsible for Zn uptake and transport across membranes (ZmZIP3, ZmHMA3, ZmHMA4) were identified, which probably form a sophisticated network to regulate the uptake, translocation, and redistribution of Zn. Additionally, we identified the genes involved in the indole-3-acetic acid (IAA) biosynthesis (ZmIGPS) and auxin-dependent gene regulation (ZmIAA). Notably, a high upregulation of ZmZIP3 was found in the Zn-deficient root of Ye478, but not in that of Wu312. Additionally, ZmZIP4, ZmZIP5, and ZmZIP7 were up-regulated in the Zn-deficient roots of Ye478 and Wu312. Our findings provide a new insight into the genetic basis of Zn deficiency tolerance.

Iron (Fe) is a mineral micronutrient for plants, and Fe deficiency is a major abiotic stress in crop production because of its low solubility under aerobic and alkaline conditions. In this study, 18 maize inbred lines were used to preliminarily illustrate the physiological mechanism underlying Fe deficiency tolerance. Then biparental linkage analysis was performed to identify the quantitative trait loci (QTLs) and candidate genes associated with Fe deficiency tolerance using the recombinant inbred line (RIL) population derived from the most Fe-efficient (Ye478) and Fe-inefficient (Wu312) inbred lines. A total of 24 QTLs was identified under different Fe nutritional status in the Ye478 × Wu312 RIL population, explaining 6.1–26.6% of phenotypic variation, and ten candidate genes were identified. Plants have evolved two distinct mechanisms to solubilize and transport Fe to acclimate to Fe deficiency, including reduction-based strategy (strategy I) and chelation-based strategy (strategy II), and maize uses strategy II. However, not only genes involved in Fe homeostasis verified in strategy II plants (strategy II genes), which included ZmYS1, ZmYS3, and ZmTOM2, but also several genes associated with Fe homeostasis in strategy I plants (strategy I genes) were identified, including ZmFIT, ZmPYE, ZmILR3, ZmBTS, and ZmEIN2. Furthermore, strategy II gene ZmYS1 and strategy I gene ZmBTS were significantly upregulated in the Fe-deficient roots and shoots of maize inbred lines, and responded to Fe deficiency more in shoots than in roots. Under Fe deficiency, greater upregulations of ZmYS1 and ZmBTS were observed in Fe-efficient parent Ye478, not in Fe-inefficient parent Wu312. Beyond that, ZmEIN2 and ZmILR3, were found to be Fe deficiency-inducible in the shoots. These findings indicate that these candidate genes may be associated with Fe deficiency tolerance in maize. This study demonstrates the use of natural variation to identify important Fe deficiency-regulated genes and provides further insights for understanding the response to Fe deficiency stress in maize.

Iron (Fe) is a limiting factor in crop growth and nutritional quality because of its low solubility. However, the current understanding of how major crops respond to Fe deficiency and the genetic basis remains limited. In the present study, Fe-efficient inbred line Ye478 and Fe-inefficient inbred line Wu312 and their recombinant inbred line (RIL) population were utilized to reveal the physiological and genetic responses of maize to low Fe stress. Compared with the Fe-sufficient conditions (+Fe: 200 μM), Fe-deficient supply (−Fe: 30 μM) significantly reduced shoot and root dry weights, leaf SPAD of Fe-efficient inbred line Ye478 by 31.4, 31.8, and 46.0%, respectively; decreased Fe-inefficient inbred line Wu312 by 72.0, 45.1, and 84.1%, respectively. Under Fe deficiency, compared with the supply of calcium nitrate (N1), supplying ammonium nitrate (N2) significantly increased the shoot and root dry weights of Wu312 by 37.5 and 51.6%, respectively; and enhanced Ye478 by 23.9 and 45.1%, respectively. Compared with N1, N2 resulted in a 70.0% decrease of the root Fe concentration for Wu312 in the −Fe treatment, N2 treatment reduced the root Fe concentration of Ye478 by 55.8% in the −Fe treatment. These findings indicated that, compared with only supplying nitrate nitrogen, combined supply of ammonium nitrogen and nitrate nitrogen not only contributed to better growth in maize but also significantly reduced Fe concentration in roots. In linkage analysis, ten quantitative trait loci (QTLs) associated with Fe deficiency tolerance were detected, explaining 6.2–12.0% of phenotypic variation. Candidate genes considered to be associated with the mechanisms underlying Fe deficiency tolerance were identified within a single locus or QTL co-localization, including ZmYS3, ZmPYE, ZmEIL3, ZmMYB153, ZmILR3 and ZmNAS4, which may form a sophisticated network to regulate the uptake, transport and redistribution of Fe. Furthermore, ZmYS3 was highly induced by Fe deficiency in the roots; ZmPYE and ZmEIL3, which may be involved in Fe homeostasis in strategy I plants, were significantly upregulated in the shoots and roots under low Fe stress; ZmMYB153 was Fe-deficiency inducible in the shoots. Our findings will provide a comprehensive insight into the physiological and genetic basis of Fe deficiency tolerance.