You’ll still need to provide your third-party account recovery password before you can use those accounts to generate passcodes. The Duo Mobile accounts list shows your restored Duo accounts, and you may use them to log into Duo-protected services with Duo Push or a generated passcode. Remember, Duo Support can’t recover your third-party accounts for you or reset your third-party recovery password. If you didn’t enable backups for your third-party accounts when you added the first one, you can do it at any time. You’ll need to provide it again to recover these accounts. Duo Mobile cannot recover access to those accounts without a backup.
If you can’t open Duo Mobile on your old device, for example, if your phone was lost or damaged, contact your Duo administrator to discuss your account recovery options. You must have access to Duo Mobile on your old Android device in order to use Instant Restore to restore your Duo-protected account backup to your new device. When you return to the accounts list after a successful third-party accounts restore, you’ll be able to tap your third-party accounts to generate passcodes for logging into those services.
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This process doesn’t reconnect any third-party accounts. To use Instant Restore you must have previously backed up your device with iCloud (with iCloud Keychain on) or an encrypted iTunes or Finder backup. If you lose this password you’ll need to manually reconnect your third-party accounts by visiting each of those services individually and following their 2FA setup process. When Duo Mobile detects you have a third-party account, you’ll be prompted to create a recovery password. Due to how apps are automatically backed up in iOS, the backup functionality of Duo Restore is always on for iOS users who have iCloud enabled and they will not see a notification indicating their information is being backed up.
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Here we show that compromising overall microRNA (miRNA) functions or mutating certain individual miRNAs impairs the long-term survival of nematodes during starvation-induced L1 diapause. Third-party accounts will also be restored if third-party backup was enabled on the old device. If you become locked out of those services and don’t have a backup of your accounts in Duo Mobile, you’ll need to contact the support team for that application (or perform the account recovery process for each of those third-party applications). However, whether an account can be restored depends upon Duo Restore being enabled by the administrator in the Duo Admin Panel or whether you’ve set a recovery password for reconnecting third-party accounts.
Individual GFP reporter constructs for candidate genes (4 ng/μL) and the mCherry internal control plasmid (4 ng/μL) were mixed with unc-119 rescuing plasmid (20 ng/μL) and pBluescript KS+ (72 ng/μL) and coinjected into unc-119(ed3) and mir-71(n4115); unc-119(ed3) worms following standard protocols (32). Knocking down lit-1 by RNAi in mir-71(lf); lin-42(lf) double mutants caused no significant suppression of the VPC timing defects of mir-71(lf) worms. To determine the functional relationship of miR-71 with LIN-42 and LIT-1, mir-71(lf); lin-42(lf) L1 worms were starved for 4 d and recovered on lit-1(RNAi) plates.
We further examined worms recovering from 4 d of L1 starvation and found that around 90% of the mir-71(lf) mutants displayed retarded vulval precursor cell (VPC) division, compared with less than 5% in wild type (Fig. 4A). We found that the 3′UTRs of several genes of the InsR pathway, including unc-31, age-1, pdk-1, akt-2, and sgk-1, contain predicted miR-71 targeting sites (as predicted by TargetScan and mirWIP). (H and I) Fluorescence images (H) and statistical data (I) showing that the M cell diveded in fed animals but remained undivided in 4-, 7-, or 11-d–starved L1 wild-type and mir-71(lf) worms. (E) Fluorescence and DIC images showing that the unc-31 3′UTR reporter was repressed in mir-71(+)worms (2/2 transgenic lines) but not in mir-71(lf) worms (4/4 transgenic lines). We found that the poor survival rate of daf-16(mu86)(lf) was further decreased by mir-71(lf) (Fig. 2C), consistent with the notion that a portion of miR-71 activities regulate genes that act in parallel to UNC-31–mediated InsR/PI3K signaling for long-term survival during L1 diapause. Mutating miR-71 drastically reduces the survival rate of animals in L1 diapause, and the effect can be suppressed by mutations of insulin receptor pathway genes age-1 and unc-31.
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